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Archive for the ‘Immune System’ Category

Gut flora – Wikipedia, the free encyclopedia

Thursday, August 4th, 2016

Gut flora (gut microbiota, or gastrointestinal microbiota) is the complex community of microorganisms that live in the digestive tracts of humans and other animals, including insects. The gut metagenome is the aggregate of all the genomes of gut microbiota.[1] The gut is one niche that human microbiota inhabit.[2]

In humans, the gut microbiota has the largest numbers of bacteria and the greatest number of species compared to other areas of the body.[3] In humans the gut flora is established at one to two years after birth, and by that time the intestinal epithelium and the intestinal mucosal barrier that it secretes have co-developed in a way that is tolerant to, and even supportive of, the gut flora and that also provides a barrier to pathogenic organisms.[4][5]

The relationship between gut flora and humans is not merely commensal (a non-harmful coexistence), but rather a mutualistic relationship.[2]:700 Human gut microorganisms benefit the host by collecting the energy from the fermentation of undigested carbohydrates and the subsequent absorption of short-chain fatty acids (SCFAs), acetate, butyrate, and propionate.[3][6] Intestinal bacteria also play a role in synthesizing vitamin B and vitamin K as well as metabolizing bile acids, sterols, and xenobiotics.[2][6] The systemic importance of the SCFAs and other compounds they produce are like hormones and the gut flora itself appears to function like an endocrine organ,[6] and dysregulation of the gut flora has been correlated with a host of inflammatory and autoimmune conditions.[3][7]

The composition of human gut flora changes over time, when the diet changes, and as overall health changes.[3][7]

The microbial composition of the gut flora varies across the digestive tract. In the stomach and small intestine, relatively few species of bacteria are generally present.[8][9] The colon, in contrast, contains a densely-populated microbial ecosystem with up to 1012 cells per gram of intestinal content.[8] These bacteria represent between 300 and 1000 different species.[8][9] However, 99% of the bacteria come from about 30 or 40 species.[10] As a consequence of their abundance in the intestine, bacteria also make up to 60% of the dry mass of feces.[11]Fungi, archaea, and viruses are also present in the gut flora, but less is known about their activities.[12]

Over 99% of the bacteria in the gut are anaerobes, but in the cecum, aerobic bacteria reach high densities.[2] It is estimated that these gut flora have around a hundred times as many genes in aggregate as there are in the human genome.[13]

Many species in the gut have not been studied outside of their hosts because most cannot be cultured.[9][10][14] While there are a small number of core species of microbes shared by most individuals, populations of microbes can vary widely among different individuals.[15] Within an individual, microbe populations stay fairly constant over time, even though some alterations may occur with changes in lifestyle, diet and age.[8][16] The Human microbiome project has set out to better describe the microflora of the human gut and other body locations.

The four dominant phyla in the human gut are Firmicutes, Bacteroidetes, Actinobacteria, and Proteobacteria.[17] Most bacteria belong to the genera Bacteroides, Clostridium, Faecalibacterium,[8][10]Eubacterium, Ruminococcus, Peptococcus, Peptostreptococcus, and Bifidobacterium.[8][10] Other genera, such as Escherichia and Lactobacillus, are present to a lesser extent.[8] Species from the genus Bacteroides alone constitute about 30% of all bacteria in the gut, suggesting that this genus is especially important in the functioning of the host.[9]

The currently known genera of fungi of the gut flora include Candida, Saccharomyces, Aspergillus, and Penicillium.

Archaea constitute another large class of gut flora which are important in the metabolism of the bacterial products of fermentation.

An enterotype is a classification of living organisms based on its bacteriological ecosystem in the human gut microbiome not dictated by age, gender, body weight, or national divisions.[18] There are indications that long-term diet influences enterotype.[19] Three human enterotypes have been discovered.[18][20]

Due to the high acidity of the stomach, most microorganisms cannot survive. The main bacterial inhabitants of the stomach include: Streptococcus, Staphylococcus, Lactobacillus, Peptostreptococcus, and types of yeast.[2]:720Helicobacter pylori is a Gram-negative spiral organism that establishes on gastric mucosa causing chronic gastritis and peptic ulcer disease and is a carcinogen for gastric cancer.[2]:904

The small intestine contains a trace amount of microorganisms due to the proximity and influence of the stomach. Gram positive cocci and rod shaped bacteria are the predominant microorganisms found in the small intestine.[2] However, in the distal portion of the small intestine alkaline conditions support gram-positive bacteria of the Enterobacteriaceae.[2] The bacterial flora of the small intestine aid in a wide range of intestinal functions. The bacterial flora provide regulatory signals that enable the development and utility of the gut. Overgrowth of bacteria in the small intestine can lead to intestinal failure.[21] In addition the large intestine contains the largest bacterial ecosystem in the human body.[2] Factors that disrupt the microorganism population of the large intestine include antibiotics, stress, and parasites.[2]

Bacteria make up most of the flora in the colon[22] and 60% of the dry mass of feces.[8] This fact makes feces an ideal source to test for gut flora for any tests and experiments by extracting the nucleic acid from fecal specimens, and bacterial 16S rRNA gene sequences are generated with bacterial primers. This form of testing is also often preferable to more invasive techniques, such as biopsies. Somewhere between 300[8] and 1000 different species live in the gut,[9] with most estimates at about 500.,[23][24] However, it is probable that 99% of the bacteria come from about 30 or 40 species, with Faecalibacterium prausnitzii being the most common species in healthy adults.[10][25]Fungi and protozoa also make up a part of the gut flora, but little is known about their activities.

Research suggests that the relationship between gut flora[26] and humans is not merely commensal (a non-harmful coexistence), but rather is a mutualistic, symbiotic relationship.[9] Though people can (barely) survive with no gut flora,[23] the microorganisms perform a host of useful functions, such as fermenting unused energy substrates, training the immune system via end products of metabolism like propionate and acetate, preventing growth of harmful species, regulating the development of the gut, producing vitamins for the host (such as biotin and vitamin K), and producing hormones to direct the host to store fats.[2]:713ff Extensive modification and imbalances of the gut microbiota and its microbiome or gene collection are associated with obesity.[27] However, in certain conditions, some species are thought to be capable of causing disease by causing infection or increasing cancer risk for the host.[8][22]

It has been demonstrated that there are common patterns of microbiome composition evolution during life.[29] In general, the diversity of microbiota composition of fecal samples is significantly higher in adults than in children, although interpersonal differences are higher in children than in adults.[30] Much of the maturation of microbiota into an adult-like configuration happens during the three first years of life.[30]

As the microbiome composition changes, so does the composition of bacterial proteins produced in the gut. In adult microbiomes, a high prevalence of enzymes involved in fermentation, methanogenesis and the metabolism of arginine, glutamate, aspartate and lysine have been found. In contrast, in infant microbiomes the dominant enzymes are involved in cysteine metabolism and fermentation pathways.[30]

Studies and statistical analyses have identified the different bacterial genera in gut microbiota and their associations with nutrient intake. Gut microflora is mainly composed of three enterotypes: Prevotella, Bacteroides, and Ruminococcus. There is an association between the concentration of each microbial community and diet. For example, Prevotella is related to carbohydrates and simple sugars, while Bacteroides is associated with proteins, amino acids, and saturated fats. One enterotype will dominate depending on the diet. Altering the diet will result in a corresponding change in the numbers of species.[19]

Malnourished human children have less mature and less diverse gut microbiota than healthy children, and changes in the microbiome associated with nutrient scarcity can in turn be a pathophysiological cause of malnutrition.[31][32] Malnourished children also typically have more potentially pathogenic gut flora, and more yeast in their mouths and throats.[33]

Gut microbiome composition depends on the geographic origin of populations. Variations in trade off of Prevotella, the representation of the urease gene, and the representation of genes encoding glutamate synthase/degradation or other enzymes involved in amino acids degradation or vitamin biosynthesis show significant differences between populations from USA, Malawi or Amerindian origin.[30]

The US population has a high representation of enzymes encoding the degradation of glutamine and enzymes involved in vitamin and lipoic acid biosynthesis; whereas Malawi and Amerindian populations have a high representation of enzymes encoding glutamate synthase and they also have an overrepresentation of -amylase in their microbiomes. As the US population has a diet richer in fats than Amerindian or Malawian populations which have a corn-rich diet, the diet is probably a main determinant of gut bacterial composition.[30]

Further studies have indicated a large difference in the composition of microbiota between European and rural African children. The fecal bacteria of children from Florence were compared to that of children from the small rural village of Boulpon in Burkina Faso. The diet of a typical child living in this village is largely lacking in fats and animal proteins and rich in polysaccharides and plant proteins. The fecal bacteria of European children was dominated by Firmicutes and showed a marked reduction in biodiversity, while the fecal bacteria of the Boulpon children was dominated by Bacteroidetes. The increased biodiversity and different composition of gut flora in African populations may aid in the digestion of normally indigestible plant polysaccharides and also may result in a reduced incidence of non-infectious colonic diseases.[34]

On a smaller scale, it has been shown that sharing numerous common environmental exposures in a family is a strong determinant of individual microbiome composition. This effect has no genetic influence and it is consistently observed in culturally different populations.[30]

In humans, a gut flora similar to an adult's is formed within one to two years of birth.[4] The gastrointestinal tract of a normal fetus has been considered to be sterile, however recently it has been acknowledged that microbial colonisation may occur in the fetus.[35] During birth and rapidly thereafter, bacteria from the mother and the surrounding environment colonize the infant's gut.[4] As of 2013, it was unclear whether most of colonizing arise from the mother or not.[4] Infants born by caesarean section may also be exposed to their mothers' microflora, but the initial exposure is most likely to be from the surrounding environment such as the air, other infants, and the nursing staff, which serve as vectors for transfer.[36] During the first year of life, the composition of the gut flora is generally simple and it changes a great deal with time and is not the same across individuals.[4]

The initial bacterial population are generally facultative anaerobic organisms; investigators believe that these initial colonizers decrease the oxygen concentration in the gut, which in turn allows purely aneorobic bacteria like Bacteroides, Actinobacteria, and Firmicutes to become established and thrive.[4] Breast-fed babies become dominated by bifidobacteria, possibly due to the contents of bifidobacterial growth factors in breast milk.[37][38] In contrast, the microbiota of formula-fed infants is more diverse, with high numbers of Enterobacteriaceae, enterococci, bifidobacteria, Bacteroides, and clostridia.[39]

Bacteria in the gut fulfill a host of useful functions for humans, including digestion of unutilized energy substrates,[40] stimulating cell growth, repressing the growth of harmful microorganisms, training the immune system to respond only to pathogens, and defending against some diseases.[8][9][41]

Without gut flora, the human body would be unable to utilize some of the undigested carbohydrates it consumes, because some types of gut flora have enzymes that human cells lack for breaking down certain polysaccharides.[6] Rodents raised in a sterile environment and lacking in gut flora need to eat 30% more calories just to remain the same weight as their normal counterparts.[6] Carbohydrates that humans cannot digest without bacterial help include certain starches, fiber, oligosaccharides, and sugars that the body failed to digest and absorb like lactose in the case of lactose intolerance and sugar alcohols, mucus produced by the gut, and proteins.[3][6]

Bacteria turn carbohydrates they ferment into short-chain fatty acids (SCFAs)[10][24] by a form of fermentation called saccharolytic fermentation.[24] Products include acetic acid, propionic acid and butyric acid.[10][24] These materials can be used by host cells, providing a major source of useful energy and nutrients for humans,[24] as well as helping the body to absorb essential dietary minerals such as calcium, magnesium and iron.[8] Gases and organic acids, such as lactic acid, are also produced by saccharolytic fermentation.[10] Acetic acid is used by muscle, propionic acid helps the liver produce ATP, and butyric acid provides energy to gut cells and may prevent cancer.[24] Evidence also indicates that bacteria enhance the absorption and storage of lipids[9] and produce and then facilitate the body to absorb needed vitamins like vitamin K.

Another benefit of SCFAs is that they increase growth of intestinal epithelial cells and control their proliferation and differentiation.[8] They may also cause lymphoid tissue near the gut to grow. Bacterial cells also alter intestinal growth by changing the expression of cell surface proteins such as sodium/glucose transporters.[9] In addition, changes they make to cells may prevent injury to the gut mucosa from occurring.[41]

In humans, a gut flora similar to an adult's is formed within one to two years of birth.[4] As the gut flora gets established, the lining of the intestines - the intestinal epithelium and the intestinal mucosal barrier that it secretes - develop as well, in a way that is tolerant to, and even supportive of, commensurate microorganisms to a certain extent and also provides a barrier to pathogenic ones.[4] Specifically, goblet cells that produce the muscosa proliferate, and the mucosa layer thickens, providing an outside mucosal layer in which "friendly" microorganisms can anchor and feed, and an inner layer that even these organisms cannot penetrate.[4][5] Additionally, the development of gut-associated lymphoid tissue (GALT), which forms part of the intestinal epithelium and which detects and reacts to pathogens, appears and develops during the time that the gut flora develops and established.[4] The GALT that develops is tolerant to gut flora species, but not to other microorganisms.[4] GALT also normally becomes tolerant to food to which the infant is exposed, as well as digestive products of food, and gut flora's metabolites produced from food.[4]

The human immune system creates cytokines that can drive the immune system to produce inflammation in order to protect itself, and that can tamp down the immune response to maintain homeostasis and allow healing after insult or injury.[4] Different bacterial species that appear in gut flora have been shown to be able to drive the immune system to create cytokines selectively; for example Bacteroides fragilis and some Clostridia species appear to drive an anti-inflammatory response, while some segmented filamentous bacteria drive the production of inflammatory cytokines.[4][42] Gut flora can also regulate the production of antibodies by the immune system.[4][43] These cytokines and antibodies can have effects outside the gut, in the lungs and other tissues.[4]

The resident gut microflora positively control the intestinal epithelial cell differentiation and proliferation through the production of short-chain fatty acids. They also mediate other metabolic effects such as the syntheses of vitamins like biotin and folate, as well as absorption of ions including magnesium, calcium and iron.[16]Methanogenic archae such as Methanobrevibacter smithii are involved in the removal of end products of bacterial fermentation such as hydrogen.[2]

Altering the numbers of gut bacteria, for example by taking broad-spectrum antibiotics, may affect the host's health and ability to digest food.[44] Antibiotics can cause antibiotic-associated diarrhea (AAD) by irritating the bowel directly, changing the levels of gut flora, or allowing pathogenic bacteria to grow.[10] Another harmful effect of antibiotics is the increase in numbers of antibiotic-resistant bacteria found after their use, which, when they invade the host, cause illnesses that are difficult to treat with antibiotics.[44]

Changing the numbers and species of gut flora can reduce the body's ability to ferment carbohydrates and metabolize bile acids and may cause diarrhea. Carbohydrates that are not broken down may absorb too much water and cause runny stools, or lack of SCFAs produced by gut flora could cause the diarrhea.[10]

A reduction in levels of native bacterial species also disrupts their ability to inhibit the growth of harmful species such as C. difficile and Salmonella kedougou, and these species can get out of hand, though their overgrowth may be incidental and not be the true cause of diarrhea.[8][10][44] Emerging treatment protocols for C. difficile infections involve fecal microbiota transplantation of donor feces. (see Fecal transplant). Initial reports of treatment describe success rates of 90%, with few side effects. Efficacy is speculated to result from restoring bacterial balances of bacteroides and firmicutes classes of bacteria.[45]

Gut flora composition also changes in severe illnesses, due not only to antibiotic use but also to such factors as ischemia of the gut, failure to eat, and immune compromise. Negative effects from this have led to interest in selective digestive tract decontamination (SDD), a treatment to kill only pathogenic bacteria and allow the re-establishment of healthy ones.[46]

Antibiotics alter the population of the gastrointestinal (GI) tract microbiota, may change the intra-community metabolic interactions, modify caloric intake by using carbohydrates, and globally affects host metabolic, hormonal and immune homeostasis.[47]

Probiotics are microorganisms that are believed to provide health benefits when consumed.[48][49] With regard to gut flora, prebiotics are typically non-digestible, fiber compounds that pass undigested through the upper part of the gastrointestinal tract and stimulate the growth or activity of advantageous gut flora by acting as substrate for them.[24][50]

Synbiotics refers to food ingredients or dietary supplements combining probiotics and prebiotics in a form of synergism.[51]

The term "pharmabiotics" is used in various ways, to mean: pharmaceutical formulations (standardized manufacturing that can obtain regulatory approval as a drug) of probiotics, prebiotics, or synbiotics;[52] probiotics that have been genetically engineered or otherwise optimized for best performance (shelf life, survival in the digestive tract, etc.);[53] and the natural products of gut flora metabolism (vitamins, etc.).[54]

There is some evidence that treatment with some probiotic strains of bacteria may be effective in irritable bowel syndrome and chronic idiopathic constipation. Those organisms most likely to result in a decrease of symptoms have included:

Gram positive bacteria present in the lumen may be associated with extending the duration of relapse for ulcerative colitis.[56]

Women's gut microbiota change as pregnancy advances, with the changes similar to those seen in metabolic syndromes such as diabetes. The change in gut flora causes no ill effects. The newborn's gut biota resemble the mother's first-trimester samples. The diversity of the flora decreases from the first to third trimester, as the numbers of certain species go up.[58]

Weight loss initiates a shift in the bacteria phyla that compose gut flora. Specifically, Bacteroidetes increase nearly linearly as weight loss progresses.[59] While there is a high level of variation in bacteria species found among individual people, this trend is prominent and distinct in humans.[60]

Bacteria in the digestive tract can contribute to disease in various ways. The presence or overabundance of some kinds of bacteria may contribute to inflammatory disorders such as inflammatory bowel disease.[8] Additionally, metabolites from certain members of the gut flora may influence host signaling pathways, contributing to disorders such as obesity and colon cancer.[8] Alternatively, in the event of a breakdown of the gut epithelium, the intrusion of gut flora components into other host compartments can lead to sepsis.[8]

Some genera of bacteria, such as Bacteroides and Clostridium, have been associated with an increase in tumor growth rate, while other genera, such as Lactobacillus and Bifidobacteria, are known to prevent tumor formation.[8]

As the liver is fed directly by the portal vein, whatever crosses the intestinal epithelium and the intestinal mucosal barrier enters the liver, as do cytokines generated there.[61] Dysbiosis in the gut flora has been linked with the development of cirrhosis and non-alcoholic fatty liver disease.[61]

Normally-commensal bacteria can be very harmful to the host if they get outside of the intestinal tract.[4][5]Translocation, which occurs when bacteria leave the gut through its mucosal lining, the border between the lumen of the gut and the inside of the body, can occur in a number of different diseases, and can be caused by too much growth of bacteria in the small intestine, reduced immunity of the host, or increased gut lining permeability.[5]

If the gut is perforated, bacteria can invade the body, causing a potentially fatal infection. Aerobic bacteria can make an infection worse by using up all available oxygen and creating an environment favorable to anaerobes.[2]:715

In a similar manner, Helicobacter pylori can cause stomach ulcers by crossing the epithelial lining of the stomach. Here the body produces an immune response. During this response parietal cells are stimulated and release extra hydrochloric acid (HCl+) into the stomach. However, the response does not stimulate the mucus-secreting cells that protect and line the epithelium of the stomach. The extra acid sears holes into the epithelial lining of the stomach, resulting in stomach ulcers.[29]

Inflammatory bowel diseases, Crohn's disease and ulcerative colitis, are all chronic inflammatory disorders of the gut, and asthma and diabetes have been described as inflammatory disorders as well; the causes of these disease are unknown and issues with the gut flora and its relationship with the host have been implicated in these conditions.[7][62][63][64]

Two hypotheses have been posed to explain the rising prevalence of these diseases in the developed world: the hygiene hypothesis, which posits that children in the developed world are not exposed to a wide enough range of pathogens and end up with an overreactive immune system, and the role of the Western pattern diet which lacks whole grains and fiber and has an overabundance of simple sugars.[7] Both hypotheses converge on the changes in the gut flora and its role in modulating the immune system, and as of 2016 this was an active area of research.[7]

Similar hypotheses have been posited for the rise of food and other allergies.[65]

As of 2016 it is not clear if changes to the gut flora cause these auto-immune and inflammatory disorders or are a product of them or adaptation to them.[7][66]

The gut flora has also been implicated in obesity and metabolic syndrome due to the key role it plays in the digestive process; the Western pattern diet appears to drive and maintain changes in the gut flora that in turn change how much energy is derived from food and how that energy is used.[64][67]

Aside from mammals, some insects also possess complex and diverse gut microbiota that play key nutritional roles.[68] Microbial communities associated termites can constitute a majority of the weight of the individuals and perform important roles in the digestion of lignocellulose and nitrogen fixation.[69] These communities are host-specific, and closely related insect species share comparable similarities in gut microbiota composition.[70][71] In cockroaches, gut microbiota have been shown to assemble in a deterministic fashion, irrespective of the inoculum;[72] the reason for this host-specific assembly remains unclear. Bacterial communities associated with insects like termites and cockroaches are determined by a combination of forces, primarily diet, but there is some indication that host phylogeny may also be playing a role in the selection of lineages.[70][71]

For more than 51 years we have known that the administration of low doses of antibacterial agents promotes the growth of farm animals to increase weight gain.[47]

In a study performed on mice by Ilseung Cho,[47] the ratio of Firmicutes and Lachnospiraceae was significantly elevated in animals treated with subtherapeutic doses of different antibiotics. By analyzing the caloric content of faeces and the concentration of small chain fatty acids (SCFAs) in the GI tract, they concluded that the changes in the composition of microbiota lead to an increased capacity to extract calories from otherwise indigestible constituents, and to an increased production of SCFAs. These findings provide evidence that antibiotics perturb not only the composition of the GI microbiome but also its metabolic capabilities, specifically with respect to SCFAs.[47]

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Herbs for the Immune System – Blessed Maine

Thursday, August 4th, 2016

This article will introduce you to a number of herbs that can safely be relied upon to strengthen the immune system, protect you from a wide array of disease-causing organisms and assist you in maintaining vibrant and robust health.

Your immune system is an incredibly complex interaction between organs, glands, body systems, surfaces, cells and chemicals. This symphonic concert of processes requires nourishment in order to function optimally.

Many herbs and other substances are used by cultures around the world to nourish and support immunity and protect us from a multitude of disease causing micro-organisms, including influenza, the Herpes simplex virus, or fungal growths such as Candida. I know a few of these protective and immune strengthening herbs on an intimate level, and would like to introduce you to some of them here. We'll cover astragalus, usnea, sage, garlic, honey, shitake and reishi mushrooms, hyssop, and St. Johns wort.

Milk Vetch Astragalus membranaceus Astragalus has been growing in our gardens for over ten years now. It is quite hardy, and withstands even the coldest Maine winter. It grows into a large bush, quite feathery, bright green and very pretty looking, with dainty, fan-like yellow flowers in mid to late summer.

Oftentimes in nature you will find that the gifts of a plant make themselves known to you in the manner in which the plant grows, the conditions it requires, and its degree of hardiness. When a plant thrives no matter what, take a deeper look, and you may find that it will help you to do the same. Astragalus strikes me as such a plant. Rugged, resilient, strong, powerful, long-lived, graceful, and elegant.

Astragalus is a tonic and restorative food and a potent medicine plant. The Chinese have been using this plant to strengthen immunity for centuries. They say it "strengthens the exterior", or protects against illness. Known as Huang-qi, astragalus is written about in the 2,000 year old Shen Nong Ben Cao Jing, and is still considered to be one of the superior tonic roots in traditional Chinese medicine. It's name literally means yellow leader; yellow referring to the inside of the root, and leader to its medicinal potency.

Mildly sweet, and slightly warm, astragalus invigorates vital energy, is restorative, strengthens resistance, restores damaged immunity, promotes tissue regeneration, is cancer inhibiting, antiviral, adaptogenic, protects and strengthens the heart and the liver, is tonic to the lungs and enhances digestion.

Many scientific studies have verified its immune enhancing action. Astragalus is a powerful "non-specific" immune system stimulant. Instead of activating our defense system against a specific disease organism, astragalus nourishes immunity by increasing the numbers and activity of roving white blood cells, the macrophages.

As an immunostimulant, astragalus engages and activates every phase of of our immune system into heightened activity. In one study, the activity of macrophages was significantly enhanced within six hours of treatment with astragalus, and remained so for the next seventy-two hours.

In Chinese medicine astragalus roots are said to tonify the Spleen, Blood, and Chi. They are used as a tonic for the lungs, for those with pulmonary disease, frequent colds, shortness of breath, and palpitations. Astragalus is also prescribed for those who suffer from fatigue, from any source, chronic nephritis, night sweats, uterine prolapse, or prolapse of the rectum.

It's tissue regenerating and anti-inflammatory abilities make astragalus an excellent ally to heal chronic ulcerations and persistent external infections, as well as to heal hard-to-heal sores and wounds, and to drain boils and draw out pus. Astragalus processed in honey is a specific against fatigue, used to boost vital energy, to nourish the blood, and also against incontinence, bloody urine or diarrhea.

In a study conducted by the University of Texas Medical Center, in Houston, researchers compared damaged immune cells from cancer patients to healthy cells. Astragalus extracts were found to completely restore the function of the cancer patients' damaged immune cells, in some cases surpassing the health and activity of the cells from healthy individuals.

The extract of astragalus was also shown to significantly inhibit the growth of tumor cells in mice, especially when combined with lovage Ligustrum lucidum. According to a study reported in Phytotherapy Research, astragalus appears to restore immunocompetence and is potentially beneficial for cancer patients as well as those suffering with AIDS. It increases the number of stem cells present in the bone marrow and lymph tissue and stimulates their differentiation into immune competent cells, which are then released into the tissues, according to one study reported in the Journal of Traditional Chinese Medicine.

Astragalus also stimulates the production of Interferon, increases its effectiveness in treating disease, and was also found to increase the life span of human cells in culture.

Astragalus protects adrenal cortical function while undergoing chemotherapy or radiation, and helps modify the gastrointestinal toxicity in patients recieving these therapies. Chinese doctors use astragalus against chronic hepatitis, and many studies have demonstrated that astragalus protects the liver against liver-toxic drugs and anti-cancer compounds commonly used in chemotherapy, such as stilbenemide. When used as an adjunct to conventional cancer treatments, astragalus appears to increase survival rates, to increase endurance, and to be strongly liver protective.

Astragalus helps lower blood pressure, due to its ability to dilate blood vessels, and protects the heart. Scientists in the Soviet Union have shown that astragalus protects the heart muscle from damage caused by oxygen deprivation and heart attack.

According to reports in the Chinese Medical Journal, doctors at the Shanghai Institute of Cardiovascular Diseases found that astragalus showed significant activity against Coxsackie B virus, which can cause an infection of the heart called Coxsackie B viral myocarditis, and for which there is no effective treatment. In a follow-up study, researchers found that astragalus helped maintain regular heart rhythms, and beating frequency, and that Coxsackie B patients showed far less damage from the viral infection (as much as 85%).

In Chinese medicine, astragalus is often combined with codonopsis. This compound is said to strengthen the heart and increase the vital energy, while invigorating the circulation of blood throughout the body. It is also traditionally combined with ginseng, and used as a tonic against fatigue, chronic tiredness, lack of energy, enthusiasm, or appetite, and to ease "spontaneous perspiration" or hot flashes.

Japanese physicians use astragalus in combination with other herbs in the treatment of cerebral vascular disease. According to a research paper published by Zhang in 1990, adolescent brain dysfunction improved more with a Traditional Chinese Medicine formula containing astragalus in combination with codonopsis and other herbs than with Ritilin.

Integrating astragalus roots into your winter-time diet, as the Asians have been doing for years, turns out to be a very good idea. Scientists have demonstrated that astragalus will not only prevent colds, but cut their duration in half. Astragalus possesses strong antiviral properties, and in one study regenerated the bronchial cells of virus-infected mice.

Astragalus has been safely used throughout Asia for thousands of years. The Chinese typically slice astragalus roots and add them, along with other vegetables, to chicken broth to create a nourishing and tonic soup. Discard the root after cooking, and consume the broth. No toxicity from the use of astragalus has ever been shown in the millennia of its use in China.

The genus Astragalus is the largest group of flowering plants, with over 2,000 different species, most of which are found in the northern temperate regions. Plants in this genus are amazingly diverse, some are nourishing and medicinal, some useful as raw materials, and others, such as the locoweeds, are toxic. Astragalus membranaceus grows in the wild along the edges of woodlands, in thickets, open woods and grasslands. It is native to the Northeastern regions of China, but grows excellently in Maine soils and temperatures, as do most Chinese medicinal plants we've attempted to grow thus far. Astragalus appreciates deep, well drained, somewhat alkaline soil.

Seeds are easily gathered and when planted in the fall require no prior soaking. They will germinate the following spring as soon as conditions are right. The seeds have a hard seed coat, and some people nick the covering with a file, or soak the seed overnight to hasten germination. Give each plant plenty of room, as much as a foot all around, and harvest after the fourth or fifth year of growth. Use whole or sliced, fresh or dried root for tinctures, honey, infusions, syrup, or in soups.

Astragalus Tincture

St. John's wort Hypericum perforatum St. John's wort contains numerous compounds that possess documented biological actions, and are the focus of much study. Those constituents that have generated the most interest thus far, include the naphthodianthrones, hypericin and pseudohypericin, a wide range of flavonoids, including quercetin, quercitrin, amentoflavone and hyperin, and the phloroglucinols, hyperforin and adhyperforin. Also of interest to researchers are the essential oils, and xanthones.

Wise herbalists have always used the whole herb, and researchers agree, that it is an interaction between the many constituents in St. John's wort, rather than any one active ingredient, that is responsible for the wide range of beneficial actions this healing herb offers.

All parts of the herb are used medicinally, with hypericin content concentrated in the buds and flowers, and also present in top and bottom leaves, as well as the stem, though to a lesser degree.

Activity of Constituents:

Amentoflavone is antiinflammatory and antiulcer.

GABA is a sedative.

Hyperforin is an antibacterial agent active against gram-positive bacteria, is wound healing, a potential anticarcinogenic, and a neurotransmitter inhibitor.

Hypericin is strongly antiviral

Proanthocyanidins are antioxidant, antimicrobial, antiviral, and vasorelaxant.

Pseudohypericin is antiviral and

Quercitrin is a MAO inhibitor, as are the Xanthones.

Xanthones are antidepressant, antimicrobial, antiviral, diuretic, and cardiotonic.

St. John's wort is an excellent wound healer. It possesses strong antimicrobial properties, is a significant antifungal and antibacterial agent, and is especially effective against gram-positive bacteria. It inactivates Escherichia coli at dilutions of 1:400 or 1:200, and is also active against Staphloccus aureus.

Two constituents of the herb, hyperforin and adhyperforin possess antibiotic effects stronger than that of sulfonilamide.

Burns heal rapidly with the application of St. John's wort. In one study using St. Johns'wort oil, first, second, and third degree burns healed at least three times as rapidly than those treated with conventional treatments, and scaring was minimal. Orally administered St. John's wort tincture demonstrated a remarkable healing of incisions, excision and dead space wounds, and has also been shown to inhibit keloid formation.

Studies indicate St. John's wort may enhance coronary blood flow as well as hawthorn, due to the activity of the procyanidins. It significantly increases the production of nocturnal melatonin, which means taking it will help you sleep better, and feel better.

St. John's wort has also shown promise in the treatment of chronic tension headaches, and also appears to be liver-protective. It is a proven antidepressant, best used by those who are mildly to moderately depressed. It is also historically used to treat neurological conditions such as anxiety, insomnia, restlessness, irritability, neuralgia, neuroses, migraines, fibrosis, dyspepsia, and sciatica.

St. Johns wort is an ally when dealing with any fungal problem, such as candida (infusion as sitz bath), thrush (infusion as mouth wash), or an infection on the skin or nails(frequent soaks in infusion). Frequent applications of St. Johns wort oil will also help in healing these infections.

Use the oil to rub on to tired, sore, achy, painful, overworked muscles. St. Johns wort oil is legendary for relieving the pain and inflammation of back-ache, stiff neck, sore shoulders, bad knees, tennis elbow, and anything else that hurts.

St. Johns'wort has shown to be of considerable benefit to patients with Acquired Immune Deficiency Syndrome. (AIDS)

In one study, 16 out of 18 patients stabilized or improved during a 40 month period during which they were treated with St. John's wort. Only 2 of the 16 experienced an opportunistic infection during the time they took the herb.

Many studies have proven that St. John's wort inhibits a variety of viruses, including herpes simplex types 1 and 2, and HIV-1 viruses associated with AIDS. Researchers have concluded that both hypericin and pseudohypericin are uncommonly effective antiviral agents.

The antiviral activity of St. John's wort appears to be somewhat photo-dynamic, involving a photoactivation process to become more intensely effective. Internal use of St. John'swort is not recommended if you are currently taking a pharmaceutical antidepressant.

St. John's wort Tincture

St. John's wort Oil

Sage Salvia officinalis The ancients used aromatic sage to bring the virtues of wisdom, strength and clear thinking. Modern day researchers in Great Britain found that sage inhibits the breakdown of acetylcholine, and so helps to preserve the compound used to prevent and treat Alzheimers.

Sage is loaded with antioxidants, so is anti-aging, and also offers lots of calcium, magnesium, the essential oil, thujone, flavonoids and phytosterols. It is sedating and soothing, and has a tonic effect on the nerves.

Sage is a potent broad spectrum antibiotic, and immune stimulant. It possesses antibacterial, and antiseptic properties and is active against Streptococcus pneumoniae, Staphylococcus aureus, Haemophilus influenzae, Pseudomonas aeruginosa. E. coli, Candida albicans, Klebsiella pneumoniae, and Salmonella spp.

Some native tribes like the Mohican, commonly chewed the leaves of sage as a strengthening tonic, and people all over the world use sage to build strength and enhance vitality.

Expectorant and diaphoretic, sage is especially effective against sore throat and upper respiratory illness, and infections where there is an excess of mucous. Sage dries up secretions. Sage is also traditionally used, and effective against, dysentery. Its astringent tannins make it an ally for healing mouth sores, canker sores, bleeding gums, and gingivitis, when used as a mouth rinse. A study done in Germany showed that drinking sage infusion on an empty stomach, reduced the blood sugar levels in diabetic patients.

In Italy sage is very commonly used as a seasoning herb. One cannot help but notice the vibrant health and strength of the elder people, which I attribute, at least in part, to their copious use of sage in the diet.

Sage Tincture

Antibiotic Spray

Garlic Allium sativum

Garlic is not only antibacterial, but antiviral, antiseptic, antiparasitic, immune-stimulating, antispasmodic, hypotensive, diaphoretic, antiprotozoan, antifungal, anthelmintic, and cholagogue.

You can rely on the regular use of this spice to keep your body toned and functioning optimally. It will help keep that all-important and vital organ, the heart toned, help keep blood pressure down, as well as help lower cholesterol. Repeated studies have shown that garlic has a beneficial effect on the heart and circulatory system. Chop some into your salad, throw it, simmered in olive oil, over noodles and sprinkle with parsley.

Garlic is rich in antibiotic powers and strengthens the immune system. It is active against both gram positive and gram negative bacteria, including Shigella dysenteriae, Staphylococcus aureus, Pseudomonas aeruginosa, Candida albicans, Escherichia coli, Streptococcus spp., Salmonella spp., Camphylobacter spp., Proteus mirablis, and Bacillius anthraxis.

Garlic is also active against herpes simplex, influenza B, HIV and many other serious illnesses. Note that it is active against the food-borne pathogens so often found in commercial foods, Shigella, E. coli, and Salmonella. Garlic kills bacteria in the gastrointestinal tract immediately on contact. To treat an active intestinal bacterial infection, consume lots of raw or cooked garlic, or take garlic capsules.

Garlic in the diet has also been shown to have a beneficial effect on those dealing with cancer, stress, and fatigue. Garlic stimulates the isles of langerhans, increases insulin production, and lowers blood sugar levels, thus aids diabetics in the control of this debilitating disease.

Garlic also helps increase the senovial fluids, and so is an ally for those dealing with arthritis. The sulfur in garlic helps break up the crystallization of uric acid in the joints, and so aids in the relief of gout. Garlic stimulates the brain and has a positive effect on brain functioning, helping to keep us alert and energized. Scientists have found that garlics anti-aging properties not only slowed the destruction of brain cells, but also caused new brain neurons to branch out. An old Ukrainian recipe to keep the mind sharp includes one pound of garlic, ground and added to a jar with the juice of 24 lemons. Leave covered for one moon cycle, then take one teaspoon each night.

Honey Honey is, an ancient Islamic saying goes, the food of foods, the drink of drinks, and the remedy of remedies. The ancient Greeks, Romans and Egyptians all kept honeybees, and extolled the virtues of honey. Some call honey a sweet medicine of heaven, others, elixir of long life. I use honey everyday and you probably should too. Heres why:

Honey is a rejuvenating, revitalizing, invigorating, natural antibiotic substance created by those magical insects, bees. Bees have been called messengers of the gods, and were associated with Great Goddess since the most ancient times. Many legends hint that bees, and their special creation, honey, played a very important role in our human development. It is said that the gifts of honey are long life, good health, and reverence for spirit. Honey has an ancient reputation as a life force increasing, immune strengthening, potency promoting, aphrodisiac elixir.

Honey consists of invert sugar (fructose, dextroglucose) and other sugars. It also contains a complex assortment of enzymes, antibiotic and antimicrobial compounds, organic acids, minerals such as iron, copper, phosphorus, sulfur, potassium, manganese, magnesium, sodium, silicon, calcium, iodine, chlorine, zinc, formic acid, and high concentrations of hydrogen peroxide. Honey also contains varying degrees (it depends on what flowers and herbs the bees are taking their nectar from) of vitamin C, the entire B complex, vitamins D, E, and K, pantothenic acid, niacin, and folic acid, amino acids, hormones, alcohols, and essential oils.

Honey can, and should be, thought of as a super food. It is a live food, stores its vitamins and minerals indefinitely, and is very easily digested by the body. Honey is an all around health and vitality enhancing substance. Wildflower honey, the concentrated nectar of wildflowers, the essence of all the combined medicinal qualities of all the diverse and abundant wild herbs, is thought to be the most medicinal.. All natural, unheated honey is antibiotic, antiviral, antifungal, anti-inflammatory, anticarcinogenic, expectorant, antiallergenic, laxative, antianemic, tonic, immune stimulating, and cell regenerating.

Bees gather the nectar from flowers and store it in their stomach while transporting it back to the hive. During their transport, the dew-laden nectars become concentrated by evaporation. The nectars also combine, in some as yet unexplained way, with the bees digestive enzymes, producing entirely unique compounds. Scientists have measured over 75 different compounds in honey, some of them so complex they have yet to be identified. One thing we can identify however, is the fact that when used as a consistent additive to food and drink, honey increases vitality, energy, immunity, libido, and life force.

Honey is proven more effective than any pharmaceutical antibiotic in the treatment of stomach ulceration, gangrene, surgical wound infections, and speedy healing of surgical incisions. Honey is unsurpassed for the protection of skin grafts, corneas, blood vessels, and bones during storage and transport. In fact, honey is such an excellent preservative of living tissue that it was commonly used to keep dead bodies from decomposing while being transported back to their homeland for burial. After his death in a foreign land, Napoleon was sent home in a huge vat of honey.

The fact that fist size ulcers and third degree burns heal beautifully with frequent applications of pure raw honey is clinically proven, and something I can personally attest to. A few years ago, I got a large third degree burn on my heel during a misstep on a motorcycle tailpipe. It was a deep wound and definitely hampered my ability to get around all that summer. I soaked my burned foot morning and night in lavender and rose salts and after each soaking applied a bandage liberally smeared with pure honey directly over the burn. I kept a thick layer of honey over that burn for a couple of months, and tried as much as possible not to walk on it. Today there is barely a trace of that huge burn hole on the heel of my foot. Since that time, honey is my first treatment of choice for any burn, first, second or third degree, any wounds, no matter how deep, skin ulcers, impetigo, and infections. I just keep whatever it is covered with a thick layer of pure honey. And keep eating it by the spoonful, or drinking it in water, or as mead, depending on what you are trying to nourish and heal.

Honey is active against staph Staphylococcus aureus, strep Streptococcus spp., and Helicobacter pylori, responsible for stomach ulcers, and enterococcus. Honey is also one of my top choices for treating any respiratory condition, whether a cold, flu, or respiratory infection. Honey will be your ally against bronchitis, chronic bronchial and asthmatic problems, rhinitis and sinusitis. Those dealing with chronic fatigue, any wasting disease, a depressed immune system, will all feel the benefits of integrating this sweet medicine of the bees into their daily diets.

Syrups made with pure honey

Usnea Usnea spp. Usnea, or old man's beard as it is commonly called, is a common lichen found hanging from trees around the world. It possesses strong antibacterial and antifungal agents and is a potent immune stimulant.

Usnea has been shown to be more effective than penicillin against some bacterial strains. It completely inhibits the growth of staphylococcus aureus, streptococcus spp., and pneumonococcus organisms. Usnea is effective against tuberculosis, triconomas, candida spp., enterococcus, and various fungal strains, and has also been reported active against Salmonella typhimurium and E.coli.

Usnea is actually two plants in one. The inner plant looks like a thin white stretchy thread or rubber band, especially when wet. The outer plant gives usnea its color and grows around the inner plant. The inner part is a potent immune stimulant, the outer part strongly antibacterial.

Among the known constituents of usnea are usnic acid, protolichesterinic acid, and oreinol derivatives. Usnea is traditionally used around the world against skin infections, upper respiratory and lung infections, and vaginal infections.

It can be dusted as a powder, drank as tea or infusion, used as a wash, bath, soak, douche, or spray. Usnea is also effective in tincture form, 30-60 drops, 4 times daily to boost immunity, 6 times daily to treat an active infection. Drink 2-4 cups of infusion for acute illness. Use 10 drops in an ounce of water and use as a nasal spray to treat sinus infections.

Usnea can sometimes be irritating to delicate mucous membranes of the mouth, nose, and throat, so the tincture should always be diluted in water before using. We walk out into the woods to a big old spruce tree beautifully decorated with long strands of this unique and potent lichen which we gather to make our medicine. Usnea easily absorbs heavy toxic metals and can be potentially toxic, so gather in a clean place.

Usnea Tincture

Shitake Mushroom Lentinus edodes Reishi Ganoderma lucidum, Western reishi/artists conk Ganoderma applanatum Immune activating fungi have been used as allies against disease for millennia. Mysterious mushrooms and fungi are classed in a kingdom all their own. They cannot be called plants, as they are much more primitive, nor are they animal. Fungi actually possess some characteristics of both plant and animal.

There are many common medicinal mushrooms with immune enhancing properties, including maitake, the abundant birch polypores, turkey tails, honey mushrooms, and hens of the woods.

The polypores are commonly given to chemotherapy and radiation patients in Japan, and have been shown to increase survival rates. The body receives deep nourishment from medicinal fungi, as the nutrients and medicinal properties of mushrooms penetrates deep into the bone marrow. So much so, that some have referred to using medicinal mushrooms as herbal bone marrow transplants!

We'll take a deeper look at two of the most widely used medicinal mushrooms, shitake and reishi.

Shitake mushrooms have been used in China for thousands of years to mobilize the immune system to fight off disease. An immunostimulant, shitake increases the activity of the human immune system against any invading organism.

Antiviral, antitumor shitake has been effectively used to treat viral infections, parasites, and cancer. One of its most important constituents, lintinan, has been shown to stimulate immune competent cells, stimulate T-cell production, and increase macrophage activity.

In one study of 23 people with low killer cell activity, and associated fever and fatique for over 6 months, all responded well to taking lintinan, despite not having responded to conventional therapies, including antibiotics and antipyretics.

Studies have shown shitake to be active against viral encephalitis. It also possesses potent anti-tumor activities, and has been shown to prevent metastasis of cancer to the lungs.

Shitake mushrooms are usually added to soups and stews, cooked for about two hours, and then allowed to sit for an additional two hours. Remove the mushrooms before consuming the broth.

Called reishi in Japan, and Ling zhe in China, all the Ganodermas are powerfully immune enhancing, and adaptogens with potent anti cancer properties.

Both sweet and bitter, the Ganodermas are powerful free radical scavengers, eliminating these highly reactive chemicals from the blood stream before they can damage the DNA of healthy cells. Ganodermas are strongly cancer protective, and have been shown to actually help break down and dissolve tumors.

Ganodermas are an excellent addition to the diet of any one who is run down, has been suffering from long term stress, and has low immune function. Either of the Ganodermas effectively increases leukocyte production, promotes lymphatic health, promotes phagocytosis, stimulates T-cells, induces the generation of immunoglobulins, and promotes the multiplication of antibodies.

Scientists from the Tokyo Medical and Dental University demonstrated that the ganoderic acid in these fungi could reduce the cholesterol production in the liver by as much as 95%.

The Ganodermas are heart warming, heart opening, promote serenity, and are said to enhance spiritual powers.

Reishi and artists conk are hard and woody, and are often referred to as shelf mushrooms. They grow on the side of either dead or living trees, and are often found on birch and other hardwoods, or hemlock. Sometimes you will find them growing on the fresh stump of a recently cut or fallen tree, and sometimes on an old stump.

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Herbs for the Immune System - Blessed Maine

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Fasting for three days can regenerate entire immune system …

Thursday, August 4th, 2016

Fasting for as little as three days can regenerate the entire immune system, even in the elderly, scientists have found in a breakthrough described as "remarkable".

Although fasting diets have been criticised by nutritionists for being unhealthy, new research suggests starving the body kick-starts stem cells into producing new white blood cells, which fight off infection.

Scientists at the University of Southern California say the discovery could be particularly beneficial for people suffering from damaged immune systems, such as cancer patients on chemotherapy.

It could also help the elderly whose immune system becomes less effective as they age, making it harder for them to fight off even common diseases.

The researchers say fasting "flips a regenerative switch" which prompts stem cells to create brand new white blood cells, essentially regenerating the entire immune system.

"It gives the 'OK' for stem cells to go ahead and begin proliferating and rebuild the entire system," said Prof Valter Longo, Professor of Gerontology and the Biological Sciences at the University of California.

"And the good news is that the body got rid of the parts of the system that might be damaged or old, the inefficient parts, during the fasting.

Now, if you start with a system heavily damaged by chemotherapy or ageing, fasting cycles can generate, literally, a new immune system."

Prolonged fasting forces the body to use stores of glucose and fat but also breaks down a significant portion of white blood cells.

During each cycle of fasting, this depletion of white blood cells induces changes that trigger stem cell-based regeneration of new immune system cells.

In trials humans were asked to regularly fast for between two and four days over a six-month period.

Scientists found that prolonged fasting also reduced the enzyme PKA, which is linked to ageing and a hormone which increases cancer risk and tumour growth.

"We could not predict that prolonged fasting would have such a remarkable effect in promoting stem cell-based regeneration of the hematopoietic system," added Prof Longo.

"When you starve, the system tries to save energy, and one of the things it can do to save energy is to recycle a lot of the immune cells that are not needed, especially those that may be damaged," Dr Longo said.

"What we started noticing in both our human work and animal work is that the white blood cell count goes down with prolonged fasting. Then when you re-feed, the blood cells come back. So we started thinking, well, where does it come from?"

Fasting for 72 hours also protected cancer patients against the toxic impact of chemotherapy.

"While chemotherapy saves lives, it causes significant collateral damage to the immune system. The results of this study suggest that fasting may mitigate some of the harmful effects of chemotherapy," said co-author Tanya Dorff, assistant professor of clinical medicine at the USC Norris Comprehensive Cancer Center and Hospital.

"More clinical studies are needed, and any such dietary intervention should be undertaken only under the guidance of a physician.

"We are investigating the possibility that these effects are applicable to many different systems and organs, not just the immune system," added Prof Longo.

However, some British experts were sceptical of the research.

Dr Graham Rook, emeritus professor of immunology at University College London, said the study sounded "improbable".

Chris Mason, Professor of Regenerative Medicine at UCL, said: There is some interesting data here. It sees that fasting reduces the number and size of cells and then re-feeding at 72 hours saw a rebound.

That could be potentially useful because that is not such a long time that it would be terribly harmful to someone with cancer.

But I think the most sensible way forward would be to synthesize this effect with drugs. I am not sure fasting is the best idea. People are better eating on a regular basis.

Dr Longo added: There is no evidence at all that fasting would be dangerous while there is strong evidence that it is beneficial.

I have received emails from hundreds of cancer patients who have combined chemo with fasting, many with the assistance of the oncologists.

Thus far the great majority have reported doing very well and only a few have reported some side effects including fainting and a temporary increase in liver markers. Clearly we need to finish the clinical trials, but it looks very promising.

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Psychological Stress and the Human Immune System: A Meta …

Thursday, August 4th, 2016

Psychol Bull. Author manuscript; available in PMC 2006 Feb 7.

Published in final edited form as:

PMCID: PMC1361287

NIHMSID: NIHMS4008

Suzanne C. Segerstrom, University of Kentucky;

The present report meta-analyzes more than 300 empirical articles describing a relationship between psychological stress and parameters of the immune system in human participants. Acute stressors (lasting minutes) were associated with potentially adaptive upregulation of some parameters of natural immunity and downregulation of some functions of specific immunity. Brief naturalistic stressors (such as exams) tended to suppress cellular immunity while preserving humoral immunity. Chronic stressors were associated with suppression of both cellular and humoral measures. Effects of event sequences varied according to the kind of event (trauma vs. loss). Subjective reports of stress generally did not associate with immune change. In some cases, physical vulnerability as a function of age or disease also increased vulnerability to immune change during stressors.

Since the dawn of time, organisms have been subject to evolutionary pressure from the environment. The ability to respond to environmental threats or stressors such as predation or natural disaster enhanced survival and therefore reproductive capacity, and physiological responses that supported such responses could be selected for. In mammals, these responses include changes that increase the delivery of oxygen and glucose to the heart and the large skeletal muscles. The result is physiological support for adaptive behaviors such as fight or flight. Immune responses to stressful situations may be part of these adaptive responses because, in addition to the risk inherent in the situation (e.g., a predator), fighting and fleeing carries the risk of injury and subsequent entry of infectious agents into the bloodstream or skin. Any wound in the skin is likely to contain pathogens that could multiply and cause infection (Williams & Leaper, 1998). Stress-induced changes in the immune system that could accelerate wound repair and help prevent infections from taking hold would therefore be adaptive and selected along with other physiological changes that increased evolutionary fitness.

Modern humans rarely encounter many of the stimuli that commonly evoked fight-or-flight responses for their ancestors, such as predation or inclement weather without protection. However, human physiological response continues to reflect the demands of earlier environments. Threats that do not require a physical response (e.g., academic exams) may therefore have physical consequences, including changes in the immune system. Indeed, over the past 30 years, more than 300 studies have been done on stress and immunity in humans, and together they have shown that psychological challenges are capable of modifying various features of the immune response. In this article we attempt to consolidate empirical knowledge about psychological stress and the human immune system through meta-analysis. Both the construct of stress and the human immune system are complex, and both could consume book-length reviews. Our review, therefore, focuses on those aspects that are most often represented in the stress and immunity literature and therefore directly relevant to the meta-analysis.

Despite nearly a century of research on various aspects of stress, investigators still find it difficult to achieve consensus on a satisfactory definition of this concept. Most of the studies contributing to this review simply define stress as circumstances that most people would find stressful, that is, stressors. We adopted Elliot and Eisdorfers (1982) taxonomy to characterize these stressors. This taxonomy has the advantage of distinguishing among stressors on two important dimensions: duration and course (e.g., discrete vs. continuous). The taxonomy includes five categories of stressors. Acute time-limited stressors involve laboratory challenges such as public speaking or mental arithmetic. Brief naturalistic stressors, such as academic examinations, involve a person confronting a real-life short-term challenge. In stressful event sequences, a focal event, such as the loss of a spouse or a major natural disaster, gives rise to a series of related challenges. Although affected individuals usually do not know exactly when these challenges will subside, they have a clear sense that at some point in the future they will. Chronic stressors, unlike the other demands we have described, usually pervade a persons life, forcing him or her to restructure his or her identity or social roles. Another feature of chronic stressors is their stabilitythe person either does not know whether or when the challenge will end or can be certain that it will never end. Examples of chronic stressors include suffering a traumatic injury that leads to physical disability, providing care for a spouse with severe dementia, or being a refugee forced out of ones native country by war. Distant stressors are traumatic experiences that occurred in the distant past yet have the potential to continue modifying immune system function because of their long-lasting cognitive and emotional sequelae (Baum, Cohen, & Hall, 1993). Examples of distant stressors include having been sexually assaulted as a child, having witnessed the death of a fellow soldier during combat, and having been a prisoner of war.

In addition to the presence of difficult circumstances, investigators also use life-event interviews and life-event checklists to capture the total number of different stressors encountered over a specified time frame. Depending on the instrument, the focus of these assessments can be either major life events (e.g., getting divorced, going bankrupt) or minor daily hassles (e.g., getting a speeding ticket, having to clean up a mess in the house). With the more sophisticated instruments, judges then code stressor severity according to how the average person in similar biographical circumstances would respond (e.g., S. Cohen et al., 1998; Evans et al., 1995).

A smaller number of studies enrolled large populations of adults who were not experiencing any specific difficulty and examined whether their immune responses varied according to their reports of perceived stress, intrusive thoughts, or both. Other studies have examined stressed populations, in which a larger range of subjective responses may be detected. This work grows out of the view that peoples biological responses to stressful circumstances are heavily dependent on their appraisals of the situation and cognitive and emotional responses to it (Baum et al., 1993; Frankenhauser, 1975; Tomaka, Blascovich, Kibler, & Ernst, 1997).

As many behavioral scientists are unfamiliar with the details of the immune system, we provide a brief overview. For a more complete treatment, the reader is directed to the sources for the information presented here (Benjamini, Coico, & Sunshine, 2000; Janeway & Travers, 1997; Rabin, 1999). Critical characteristics of various immune components and assays are also listed in .

Immune Parameters Reported and Critical Characteristics

There are several useful ways of dividing elements of the immune response. For the purposes of understanding the relationship of psychosocial stressors to the immune system, it is useful to distinguish between natural and specific immunity. Natural immunity is an immune response that is characteristic not only of mammals but also lower order organisms such as sponges. Cells involved in natural immunity do not provide defense against any particular pathogen; rather, they are all-purpose cells that can attack a number of different pathogens1 and do so in a relatively short time frame (minutes to hours) when challenged. The largest group of cells involved in natural immunity is the granulocytes. These cells include the neutrophil and the macrophage, phagocytic cells that, as their name implies, eat their targets. The generalized response mounted by these cells is inflammation, in which neutrophils and macrophages congregate at the site of injury or infection, release toxic substances such as oxygen radicals that damage invaders, and phagocytose both invaders and damaged tissue. Macrophages in particular also release communication molecules, or cytokines, that have broad effects on the organism, including fever and inflammation, and also promote wound healing. These proinflammatory cytokines include interleukin(IL)-1, IL-6, and tumor necrosis factor alpha (TNF). Other granulocytes include the mast cell and the eosinophil, which are involved in parasitic defense and allergy.

Another cell involved in natural immunity is the natural killer cell. Natural killer cells recognize the lack of a self-tissue molecule on the surface of cells (characteristic of many kinds of virally infected and some cancerous cells) and lyse those cells by releasing toxic substances on them. Natural killer cells are thought to be important in limiting the early phases of viral infections, before specific immunity becomes effective, and in attacking self-cells that have become malignant.

Finally, complement is a family of proteins involved in natural immunity. Complement protein bound to microorganisms can up-regulate phagocytosis and inflammation. Complement can also aid in antibody-mediated immunity (discussed below as part of the specific immune response).

Specific immunity is characterized by greater specificity and less speed than the natural immune response. Lymphocytes have receptor sites on their cell surfaces. The receptor on each cell fits with one and only one small molecular shape, or antigen, on a given invader and therefore responds to one and only one kind of invader. When activated, these antigen-specific cells divide to create a population of cells with the same antigen specificity in a process called clonal proliferation, or the proliferative response. Although this process is efficient in terms of the number of cells that have to be supported on a day-to-day basis, it creates a delay of up to several days before a full defense is mounted, and the body must rely on natural immunity to contain the infection during this time.

There are three types of lymphocytes that mediate specific immunity: T-helper cells, T-cytotoxic cells, and B cells. The main function of T-helper cells is to produce cytokines that direct and amplify the rest of the immune response. T-cytotoxic cells recognize antigen expressed by cells that are infected with viruses or otherwise compromised (e.g., cancer cells) and lyse those cells. B cells produce soluble proteins called antibody that can perform a number of functions, including neutralizing bacterial toxins, binding to free virus to prevent its entry into cells, and opsonization, in which a coating of antibody increases the effectiveness of natural immunity. There are five kinds of antibody: Immunoglobulin (Ig) A is found in secretions, IgE binds to mast cells and is involved in allergy, IgM is a large molecule that clears antigen from the bloodstream, IgG is a smaller antibody that diffuses into tissue and crosses the placenta, and IgD is of unknown significance but may be produced by immature B cells.

An important immunological development is the recognition that specific immunity in humans is composed of cellular and humoral responses. Cellular immune responses are mounted against intracellular pathogens like viruses and are coordinated by a subset of T-helper lymphocytes called Th1 cells. In the Th1 response, the T-helper cell produces cytokines, including IL-2 and interferon gamma (IFN). These cytokines selectively activate T-cytotoxic cells as well as natural killer cells. Humoral immune responses are mounted against extracellular pathogens such as parasites and bacteria; they are coordinated by a subset of T-helper lymphocytes called Th2 cells. In the Th2 response, the T-helper cell produces different cytokines, including IL-4 and IL-10, which selectively activate B cells and mast cells to combat extracellular pathogens.

Immune assays can quantify cells, proteins, or functions. The most basic parameter is a simple count of the number of cells of different subtypes (e.g., neutrophils, macrophages), typically from peripheral blood. It is important to have an adequate number of different types of immune cells in the correct proportions. However, the normal range for these enumerative parameters is quite large, so that correct numbers and proportions can cover a wide range, and small changes are unlikely to have any clinical significance in healthy humans.

Protein productioneither of antibody or cytokinescan be measured in vitro by stimulating cells and measuring protein in the supernatant or in vivo by measuring protein in peripheral blood. For both antibody and cytokine, higher protein production may represent a more robust immune response that can confer protection against disease. Two exceptions are levels of proinflammatory cytokines (IL-1, IL-6, and TNF) and antibody against latent virus. Proinflammatory cytokines are increased with systemic inflammation, a risk factor for poorer health resulting from cardiac disease, diabetes mellitus, or osteoporosis (Ershler & Keller, 2000; Luster, 1998; Papanicoloaou, Wilder, Manolagas, & Chrousos, 1998). Antibody production against latent virus occurs when viral replication triggers the immune system to produce antibodies in an effort to contain the infection. Most people become infected with latent viruses such as Epstein-Barr virus during adolescence and remain asymptomatically infected for the rest of their lives. Various processes can activate these latent viruses, however, so that they begin actively replicating. These processes may include a breakdown in cellular immune response (Jenkins & Baum, 1995). Higher antibody against latent viruses, therefore, may indicate poorer immune control over the virus.

Functional assays, which are performed in vitro, measure the ability of cells to perform specific activities. In each case, higher values may represent more effective immune function. Neutro-phils function can be quantified by their ability to migrate in a laboratory assay and their ability to release oxygen radicals. The natural killer cytotoxicity assay measures the ability of natural killer cells to lyse a sensitive target cell line. Lymphocyte proliferation can be stimulated with mitogens that bypass antigen specificity to activate cells or by stimulating the T cell receptor.

How could stress get inside the body to affect the immune response? First, sympathetic fibers descend from the brain into both primary (bone marrow and thymus) and secondary (spleen and lymph nodes) lymphoid tissues (Felten & Felten, 1994). These fibers can release a wide variety of substances that influence immune responses by binding to receptors on white blood cells (Ader, Cohen, & Felten, 1995; Felten & Felten, 1994; Kemeny, Solomon, Morley, & Herbert, 1992; Rabin, 1999). Though all lymphocytes have adrenergic receptors, differential density and sensitivity of adrenergic receptors on lymphocytes may affect responsiveness to stress among cell subsets. For example, natural killer cells have both high-density and high-affinity 2-adrenergic receptors, B cells have high density but lower affinity, and T cells have the lowest density (Anstead, Hunt, Carlson, & Burki, 1998; Landmann, 1992; Maisel, Fowler, Rearden, Motulsky, & Michel, 1989). Second, the hypothalamicpituitaryadrenal axis, the sympatheticadrenalmedullary axis, and the hypothalamicpituitaryovarian axis secrete the adrenal hormones epinephrine, norepinephrine, and cortisol; the pituitary hormones prolactin and growth hormone; and the brain peptides melatonin, -endorphin, and enkephalin. These substances bind to specific receptors on white blood cells and have diverse regulatory effects on their distribution and function (Ader, Felten, & Cohen, 2001). Third, peoples efforts to manage the demands of stressful experience sometimes lead them to engage in behaviorssuch as alcohol use or changes in sleeping patternsthat also could modify immune system processes (Kiecolt-Glaser & Glaser, 1988). Thus, behavior represents a potentially important pathway linking stress with the immune system.

Maier and Watkins (1998) proposed an even closer relationship between stress and immune function: that the immunological changes associated with stress were adapted from the immunological changes in response to infection. Immunological activation in mammals results in a syndrome called sickness behavior, which consists of behavioral changes such as reduction in activity, social interaction, and sexual activity, as well as increased responsiveness to pain, anorexia, and depressed mood. This syndrome is probably adaptive in that it results in energy conservation at a time when such energy is best directed toward fighting infection. Maier and Watkins drew parallels between the behavioral, neuroendo-crine, and thermoregulatory responses to sickness and stress. The common thread between the two is the energy mobilization and redirection that is necessary to fight attackers both within and without.

Conceptualizations of the nature of the relationship between stress and the immune system have changed over time. Selyes (1975) finding of thymic involution led to an initial model in which stress is broadly immunosuppressive. Early human studies supported this model, reporting that chronic forms of stress were accompanied by reduced natural killer cell cytotoxicity, suppressed lymphocyte proliferative responses, and blunted humoral responses to immunization (see S. Cohen, Miller, & Rabin, 2001; Herbert & Cohen, 1993;Kiecolt-Glaser, Glaser, Gravenstein, Malarkey, & Sheridan, 1996, for reviews). Diminished immune responses of this nature were assumed to be responsible for the heightened incidence of infectious and neoplastic diseases found among chronically stressed individuals (Andersen, Kiecolt-Glaser, & Glaser, 1994; S. Cohen & Williamson, 1991).

Although the global immunosuppression model enjoyed long popularity and continues to be influential, the broad decreases in immune function it predicts would not have been evolutionarily adaptive in life-threatening circumstances. Dhabhar and McEwen (1997, 2001) proposed that acute fight-or-flight stressors should instead cause redistribution of immune cells into the compartments in which they can act the most quickly and efficiently against invaders. In a series of experiments with mice, they found that during acute stress, T cells selectively redistributed into the skin, where they contributed to enhancement of the immune response. In contrast, during chronic stress, T cells were shunted away from the skin, and the immune response to skin test challenge was diminished (Dhabhar & McEwen, 1997). On the basis of these findings they proposed a biphasic model in which acute stress enhances, and chronic stress suppresses, the immune response.

A modification of this model posits that short-term changes in all components of the immune system (natural and specific) are unlikely to occur because they would expend too much energy to be adaptive in life-threatening circumstances. Instead, stress should shift the balance of the immune response toward activating natural processes and diminishing specific processes. The premise underlying this model is that natural immune responses are better suited to managing the potential complications of life-threatening situations than specific immune responses because they can unfold much more rapidly, are subject to fewer inhibitory constraints, and require less energy to be diverted from other bodily systems that support the fight-or-flight response (Dopp, Miller, Myers, & Fahey, 2000; Sapolsky, 1998).

Even with this modification of the biphasic model, neither it nor the global immunosuppression model sufficiently explains findings that link chronic stress with both disease outcomes associated with inadequate immunity (infectious and neoplastic disease) and disease outcomes associated with excessive immune activity (allergic and autoimmune disease). To resolve this paradox, some researchers have chosen to focus on how chronic stress might shift the balance of the immune response. The most well-known of these models hypothesizes that chronic stress elicits simultaneous enhancement and suppression of the immune response by altering patterns of cytokine secretion (Marshall et al., 1998). Th1 cytokines, which activate cellular immunity to provide defense against many kinds of infection and some kinds of neoplastic disease, are suppressed. This suppression has permissive effects on production of Th2 cytokines, which activate humoral immunity and exacerbate allergy and many kinds of autoimmune disease. This shift can occur via the effects of stress hormones such as cortisol (Chiappelli, Manfrini, Franceschi, Cossarizza, & Black, 1994). Th1-to-Th2 shift changes the balance of the immune response without necessarily changing the overall level of activation or function within the system. Because a diminished Th1-mediated cellular immune response could increase vulnerability to infectious and neoplastic disease, and an enhanced Th-2 mediated humoral immune response could increase vulnerability to autoimmune and allergic diseases, this cytokine shift model also is able to reconcile patterns of stress-related immune change with patterns of stress-related disease outcomes (Marshall et al., 1998).

If the stress response in the immune system evolved, a healthy organism should not be adversely affected by activation of this response because such an effect would likely have been selected against. Although there is direct evidence that stress-related immunosuppression can increase vulnerability to disease in animals (e.g., Ben Eliyahu, Shakhar, Page, Stefanski, & Shakhar, 2000; Quan et al., 2001; Shavit et al., 1985; Sheridan et al., 1998), there is little or no evidence linking stress-related immune change in healthy humans to disease vulnerability. Even large stress-induced immune changes can have small clinical consequences because of the redundancy of the immune systems components or because they do not persist for a sufficient duration to enhance disease susceptibility. In short, the immune system is remarkably flexible and capable of substantial change without compromising an otherwise healthy host.

However, the flexibility of the immune system can be compromised by age and disease. As humans age, the immune system becomes senescent (Boucher et al., 1998; Wikby, Johansson, Ferguson, & Olsson, 1994). As a consequence, older adults are less able to respond to vaccines and mount cellular immune responses, which in turn may contribute to early mortality (Ferguson, Wikby, Maxson, Olsson, & Johansson, 1995; Wayne, Rhyne, Garry, & Goodwin, 1990). The decreased ability of the immune system to respond to stimulation is one indicator of its loss of flexibility.

Loss of self-regulation is also characteristic of disease states. In autoimmune disease, for example, the immune system treats self-tissue as an invader, attacking it and causing pathology such as multiple sclerosis, rheumatoid arthritis, Crohns disease, and lupus. Immune reactions can also be exaggerated and pathological, as in asthma, and suggest loss of self-regulation. Finally, infection with HIV progressively incapacitates T-helper cells, leading to loss of the regulation usually provided by these cells. Although each of these diseases has distinct clinical consequences, the change in the immune system from flexible and balanced to inflexible and unbalanced suggests increased vulnerability to stress-related immune dysregulation; furthermore, dysregulation in the presence of disease may have clinical consequences (e.g., Bower, Kemeny, Taylor, & Fahey, 1998).

We performed a meta-analysis of published results linking stress and the immune system. We feel that this area is in particular need of a quantitative review because of the methodological nature of most studies in this area. For practical and economic reasons, many psychoneuroimmunology studies have a relatively small sample size, creating the possibility of Type II error. Furthermore, many studies examine a broad range of immunological parameters, creating the possibility of Type I error. A quantitative review, of which meta-analysis is the best example, can better distinguish reliable effects from those arising from both Type I and Type II error than can a qualitative review.

We combined studies in such a way as to test the models of stress and immune change reviewed above. First, we examined each stressor type separately, yielding separate effects for stressors of different duration and trajectory. Second, we examined both healthy and medical populations, allowing comparison of the effects of stress on resilient and vulnerable populations; along the same lines, we also examined the effects of age. Finally, we examined all immune parameters separately so that patterns of response (e.g., global immunosuppression vs. cytokine shift) would be clearer.

Articles for the meta-analysis were identified through computerized literature searches and searches of reference lists. MEDLINE and PsycINFO were searched for the years 1960 2001. Following the example of Herbert and Cohen (1993), we used the terms stress, hassles, and life events in combination with the term immune to search both databases. The reference lists of 11 review articles on stress and the immune system (Benschop, Geenen, et al., 1998; Biondi, 2001; Cacioppo, 1994; S. Cohen & Herbert, 1996; S. Cohen et al., 2001; Herbert & Cohen, 1993; Kiecolt-Glaser, Cacioppo, Malarkey, & Glaser, 1992; Kiecolt-Glaser, McGuire, Robles, & Glaser, 2002; Maier, Watkins, & Fleshner, 1994; OLeary, 1990; Zorrilla et al., 2001) were then searched to identify additional articles.

We selected only articles that met a number of inclusion criteria. The first criterion was that the work had to include a measure of stress. This criterion could be met if a sample experiencing a stressor was compared with an unstressed control group, if a sample experiencing a stressor was compared with itself at a baseline that could reasonably be considered low stress, or if differing degrees of stress in a sample were assessed with an explicit measure of stress. This criterion was not met if, for example, anxietyan affective statewas used as a proxy for stress, or it seemed likely that a baseline assessment occurred during periods of significant stress. The second criterion was that the stressor had to be psychosocial. Stressors that included a significant physical element such as pain, cold, or physical exhaustion were eliminated (e.g., Antarctic isolation, space flight, military training). The third criterion was that the work had to include a measure of the immune system. This criterion was met by any enumerative or functional in vitro or in vivo immune assay. However, clinical disease outcomes such as HIV progression or rhinovirus infection did not meet this criterion. Finally, we eliminated articles from which a meaningful effect size could not be abstracted. For example, when between- and within-subjects observations were treated as independent, the reported effect was likely to be inflated. In a few cases, effects of stress and clinical status were confoundedthat is, a stressed clinical group was compared with an unstressed healthy groupand hence these studies were excluded from the meta-analysis.

We coded stressors in the articles into five classes: acute time-limited, brief naturalistic, event sequence, chronic, and distant. The most difficult distinctions among event sequence, chronic, and distant stressors were based on temporal and qualitative considerations. Event sequences included discrete stressors occurring 1 year or less before immune assessment and could be of any severity. These were most often normative stressors such as bereavement. Chronic stressors were ongoing stressors such as caregiving and disability. Distant stressors were severe, traumatic events that could meet the stressor criterion for posttraumatic stress disorder (American Psychiatric Association, 1994), such as combat exposure or abuse, and had happened more than 1 year before immune assessment. Most stressors in this category occurred 5 to 10 years before immune assessment. Disagreements in stressor classification were resolved by consensus. Subgroups for moderator analyses were similarly decided.

Meta-analysis is a tool for synthesizing research findings. It proceeds in two phases. In the first, effect sizes are computed for each study. An effect size represents the magnitude of the relationship between two variables, independent of sample size. In this context it can be viewed as a measure of how much two groups, one experiencing a stressor and the other not, differ on a specific immune outcome. In the second phase, effect sizes from individual studies are combined to arrive at an aggregate effect size for each immune outcome of interest.

We used Pearsons r as the effect size metric in this meta-analysis. Effect sizes for individual studies were computed using descriptive statistics presented in the original published reports. When these statistics were not available, we requested them from authors. This strategy was successful in most circumstances. To compute Pearsons r from descriptive statistics in between-subjects designs, we subtracted the control group mean from the stressed group mean and divided this value by the pooled sample standard deviation. The value that emerged from this computation, known as Cohens d, was then converted into a Pearsons r by taking the square root of the quantity d2/(d2 + 4). (See Rosenthal, 1994.) To compute Pearsons r from descriptive statistics in within-subjects designs, we subtracted the group mean at baseline from the group mean during stress and divided this quantity by the sample standard deviation at baseline. This d value was converted into a Pearsons r by taking the square root of the quantity d2/(d2 + 4). In cases in which descriptive statistics were not available, Pearsons r was computed from inferential statistics using standard formulae (Rosenthal, 1994). These formulae had to be modified slightly for studies that used within-subjects designs because effect sizes are systematically overestimated when they are calculated from repeated measures test statistics (Dunlap, Cortina, Vaslow, & Burke, 1996). In these situations we derived effect size estimates using the formula d = tc[2 (1 r)]1/2, where tc corresponds to the value of the t statistic for correlated measures, and r corresponds to the value of the correlation between outcome measures at pretest and posttest (Dunlap et al., 1996). Because very few studies reported the value of r, we used a value of .60 to compute effect sizes in this meta-analysis. This represents the average correlation between pre-stress and poststress measures of immune function in a series of studies performed in our laboratories. To ensure that the meta-analytic findings were robust to variations in r, we conducted follow-up analyses using r values ranging from .45 to .75. Very similar findings emerged from these analyses, suggesting that the values we present below are reliable estimates of effect size. If anything, they are probably conservative estimates, because the prepost correlation between immune measures often is substantially lower than .60.

The effect size estimates from individual studies were subsequently aggregated using random-effects models with the software program Comprehensive Meta-Analysis (Borenstein & Rothstein, 1999). The random-effects model views each study in a meta-analysis as a random observation drawn from a universe of potential investigations. As such, it assumes that the magnitude of the relationship between stress and the immune system differs across studies as a result of random variance associated with sampling error and differences across individuals in the processes of interest. Because of these assumptions, random-effects models not only permit one to draw inferences about studies that have been done but also to generalize to studies that might be done in the future (Raudenbush, 1994; Shadish & Haddock, 1994). It also bears noting that in the population of studies on stress and immunity there is likely to be a fair amount of nonrandom variance, as researchers who examine ostensibly similar phenomena may still differ in terms of the samples they recruit, the operational definition of stress they use, and the laboratory methods they utilize to assess a specific immune process.

Separate random-effects models were computed for each immune outcome included in the meta-analysis. Prior to computing the random-effects model, r values derived from each study were z-transformed by the software program, as recommended by Shadish and Haddock (1994), to stabilize variance. The z values were later back-transformed into r values to facilitate interpretation of the meta-analytic findings. In the end, each random-effects model yielded an aggregate weighted effect size r, which can be interpreted the same way as a correlation coefficient, ranging in value from 1.00 to 1.00. Each r statistic was weighted before aggregation by multiplying its value by the inverse of its variance; this procedure enabled larger studies to contribute to effect size estimates to a greater extent than smaller ones. Weighting effect sizes is important because larger studies provide more accurate estimates of true population parameters (Shadish & Haddock, 1994). After each aggregate effect size had been derived, we computed 95% confidence intervals around it, assessed whether it was statistically significant, and computed a heterogeneity coefficient to determine whether the studies contributing to it had yielded consistent findings. Following convention, aggregate effect sizes were considered statistically different from zero when (a) their corresponding z value was greater than 1.96 and (b) the 95% confidence intervals around them did not include the value zero (Rosenthal, 1991; Shadish & Haddock, 1994).

To determine whether the studies contributing to each aggregate effect size shared a common population value, we computed the heterogeneity statistic Q (Shadish & Haddock, 1994). This statistic is chi-square distributed with k 1 degrees of freedom, where k represents the number of independent effect sizes included. When a statistically significant heterogeneity test emerged, we searched for moderators (characteristics of the participants, stressful experience, or measurement strategy) that could explain the variability across studies. The first step in this process involved estimating correlations between participant characteristics (e.g., mean age, percentage female) and immune effects to examine whether the strength of effects varied according to demographics. When it was possible to do so, we then stratified the studies according to characteristics of the stressful experience (e.g., duration, quality) or the measurement strategy (e.g., interview, checklist), and computed separate random-effects analyses for each subgroup.

Occasionally authors of studies failed to report the descriptive or inferential statistics needed to compute an effect size. In some of these cases, the authors noted that there was a significant difference between a stressed and control group. When this occurred, we computed effect sizes assuming that p values were equivalent to .05. This represents a conservative approach because the actual p values were probably smaller. In other cases, the authors noted that a stressed and control group did not differ with respect to an immune outcome, but failed to provide any further statistical information. When this occurred, we computed effect sizes assuming that there was no difference at all between the groups (r = .00). Because there is seldom no difference at all between two groups, this also represents a conservative strategy. Imputation was used in less than 7% of cases.

The validity of a meta-analysis rests on the assumption that each value contributing an aggregate effect size is statistically independent of the others (Rosenthal, 1991). We devised a number of strategies to avoid violating this independence assumption. First, in studies that assessed stimulated-lymphocyte proliferation at multiple mitogen dosages, we computed the average effect size across mitogen dosages, and we used this value to derive aggregate indices. We used an analogous strategy for studies that assessed natural killer cell cytotoxicity at multiple effector:target cell ratios. Second, in studies that utilized designs in which multiple laboratory stressors were compared with a control condition, the average effect size across stressor conditions was computed and later used to derive aggregate indices. Because this averaging procedure in most cases yielded an effect size that was smaller than that of the most potent stressor, we also computed meta-analyses using the larger of the effect sizes from each study rather than the average. Doing so did not alter any of the substantive findings we report. Third, in studies in which immune outcomes were assessed on multiple occasions during a stressful experience, the average effect size across occasions was used to derive aggregate indices. Note that we did not conduct meta-analyses of recovery effects, that is, immune values after a stressor had ended. Although such an analysis would answer interesting questions about the stress-recovery process, there were not enough studies that included similar immune outcomes assessed at similar time points after stress to permit a complete analysis. Fourth, because some data were published in more than one outlet, we contacted authors of multiple publications to determine sample independence or dependence.

The meta-analysis is based on effect sizes derived from 293 independent studies. These studies were reported in 319 separate articles in peer-reviewed scientific journals (see ). A total of 18,941 individuals participated in these studies. Their mean age was 34.8 years (SD = 15.9). Although the studies collectively included a broad range of age groups (range = 578 years), most focused heavily on younger adults. More than half of the studies (51.3%) had a mean age under 30.0 years, and more than four fifths (84.8%) had a mean age under 55.0 years. Slightly more than two thirds of the studies (68.5%) included women; in the average study almost half (42.8%) of the participants were female. The vast majority of studies (84.8%) focused on medically healthy adults.2 Of those that included medical populations, most focused on HIV/AIDS (k = 18; 38.3%), arthritis (k = 6; 12.8%), cancer (k = 5; 10.6%), or asthma (k = 4; 8.5%).

Studies Used in the Meta-Analysis by Type of Stressor

With respect to the kinds of stressors examined by studies in the meta-analysis, the most commonly utilized models were acute laboratory challenges (k = 85; 29.0%) and brief naturalistic stressors (k = 63; 21.5%). Stressful event sequences (k = 30; 10.2%), chronic stressors (k = 23; 7.8%), and distant traumatic experiences (k = 9; 3.1%) were explored less frequently. More than a quarter of the studies in the meta-analysis modeled the stress process by administering nonspecific life-event checklists (k = 53; 18.1%) and/or global perceived stress measures (k = 21; 7.1%) to participants. A small minority of studies examined whether reports of perceived stress or intrusive memories were associated with the extent of immune dysregulation within populations who had suffered a specific traumatic experience (k = 9; 3.1%).

The studies in the meta-analysis examined 292 distinct immune system outcomes. A minority of these outcomes were assessed in three or more studies (k = 87; 30.0%), and as such, they are the focus of the meta-analyses we present in the rest of this article (see ). The most commonly assessed enumerative outcomes were counts of T-helper lymphocytes (k = 90; 30.7%), T-cytotoxic lymphocytes (k = 81; 27.6%), natural killer cells (k = 67; 22.9%), and total lymphocytes (k = 52; 17.7%). The most commonly assessed functional outcomes were natural killer cell cytotoxicity (k = 94; 32.1%) and lymphocyte proliferation stimulated by the mitogens phytohemagglutinin (PHA; k = 65; 22.2%), concanavalin A (ConA; k = 39; 13.3%), and pokeweed mitogen (PWM; k = 26; 8.9%).

lists the immune parameters analyzed with the arm of the immune system to which they belong (natural or specific) and, briefly, their function. Where relevant, cell surface markers used to identify classes of immunocytes in flow cytometry are given. For example, the cell surface marker CD19 is used to identify B lymphocytes. Recall that different models of stress and the immune system posit differential effects of stress on subsets of the immune systemfor example, natural versus specific immunity or cellular (Th1) versus humoral (Th2) immunity. acts as a guide for interpreting the pattern of results in light of these models.

In the following sections we describe the meta-analytic results for each stressor category. A useful rule of thumb for judging effect sizes is to consider values of .10, .30, and .50 as corresponding to small, medium, and large effects, respectively (J. Cohen & Cohen, 1983); more generally, the aggregate effect size r can be interpreted in the same fashion as a correlation, with values ranging from 1.00 to 1.00. Positive values indicate that the presence of a stressor increases a particular immune parameter relative to some baseline (or control) condition. We should caution the reader that in some analyses, our statistics are derived from as few as three independent studies. Although meta-analyses of small numbers of studies do not pose any major statistical problems, it is important to remember that they have limited power to detect statistically significant effect sizes. What a meta-analysis can accurately provide in these instances, however, is an estimate of how much and what direction a given stressors presence influences a specific immune outcome (i.e., an effect size estimate).

Acute time-limited stressors included primarily experimental manipulations of stressful experiences, such as public speaking and mental arithmetic, that lasted between 5 and 100 min. Reliable effects on the immune system included increases in immune parameters, especially natural immunity. The most robust effect of this kind of experience was a marked increase in the number of natural killer cells (r =.43) and large granular lymphocytes (r =.53) in peripheral blood (see ). This effect is consistent with the view that acute stressors cause immune cells to redistribute into the compartments in which they will be most effective (Dhabhar & McEwen, 1997). However, other types of lymphocytes did not show robust redistribution effects: B cells and T-helper cells showed very little change (rs = .07 and .01, respectively), and this change was not statistically significant across studies. T-cytotoxic lymphocytes did tend to increase reliably in peripheral blood, though to a lesser degree than their natural immunity counterparts (r =.20); this increase drove a reliable decline in the T-helper:T-cytotoxic ratio (r = .23). However, natural killer cells as well as T-cytotoxic cells can express CD8, the marker most often used to define the latter population. Because some studies did not use the T cell receptor (CD3) to differentiate between CD3CD8+ natural killer cells and CD3+CD8+ T-cytotoxic cells, it is possible that the effect for T-cytotoxic cells is actually being driven by natural killer cells (Benschop, Rodriguez-Feuerhahn, & Schedlowski, 1996).

Meta-Analysis of Immune Responses to Acute Time-Limited Stress in Healthy Participants

The results for cell percentages roughly parallel those for number. However, the percentage data are harder to interpret because any given parameter is linearly dependent on the other parameters: For example, the enumerative data suggest that the decrease in percentage T-helper cells (r = .24) is probably an artifact of the increases in percentage natural killer cells (r = .24) and percentage T-cytotoxic cells (r = .09).

Another effect that may be considered a redistribution effect is the significant increase in secretory IgA in saliva (r = .22). The time frame of these acute stressors is too short for the synthesis of a significant amount of new antibody; therefore, this increase is probably due to release of already-synthesized antibody from plasma cells and increased translocation of antibody across the epithelium and into saliva (Bosch, Ring, de Geus, Veerman, & Amerongen, 2002). This effect therefore represents relocation, albeit of an immune protein rather than an immune cell.

There were also a number of functional effects. First, natural killer cell cytotoxicity significantly increased with acute stressors (r = .30), but only when the concomitant increase in proportion of natural killer cells in the effector mix was not removed statistically. When examined on a per-cell basis, cytotoxicity did not significantly increase (r = .12). One could, therefore, consider the increase in cytotoxicity a methodological artifact of the definition of effector in effector:target ratios. However, to the degree that one is interested in the general cytotoxic potential of the contents of peripheral blood rather than that of a specific natural killer cell, the uncorrected value is more illustrative. Second, mitogen-stimulated proliferative responses decreased significantly. Again, this could be a methodological artifact of the mix of cells in the assay. However, the proportion of total T and B cells, which are responsible for the proliferative response to PWM and ConA, did not decrease as reliably or as much as did the proliferative response (rs = .05 to .11 vs. .10 to .17), suggesting that acute stressors do decrease this function of specific immunity. Finally, the production of two cytokines, IL-6 and IFN, was increased significantly following acute stress (rs = .28 and .21, respectively).

The data for acute stressors, therefore, support an upregulation of natural immunity, as reflected by increased number of natural killer cells in peripheral blood, and potential downregulation of specific immunity, as reflected by decreased proliferative responses. Other indicators of upregulated natural immunity include increased neutrophil numbers in peripheral blood (r = .30), increased production of a proinflammatory cytokine (IL-6), and increased production of a cytokine that potently stimulates macrophages and natural killer cells as well as T cells (IFN). The only exception to this pattern was the increased secretion of IgA antibody, which is a product of the specific immune response. An interesting question for future research is whether this effect is part of a larger nonspecific protein release in the oral cavity in response to acute stress (cf. Bosch et al., 2002).

It bears noting that a number of the findings presented in are accompanied by significant heterogeneity statistics. To identify moderating variables that might explain some of this heterogeneity, we examined whether effect sizes varied according to demographic characteristics of the sample (mean age and percentage female) or features of the acute challenge (its duration and nature). Neither of the demographic characteristics showed a consistent relationship with immune outcomes. Although these findings suggest that acute time-limited stressors elicit a similar pattern of immune response for men and women across the life span, this conclusion needs to be viewed somewhat cautiously given the narrow range of ages found in these studies. We also did not find a consistent pattern of relationships between features of the acute challenge and immune outcomes. Acute stressors elicited similar patterns of immune change across a wide spectrum of durations ranging from 5 though 100 min and irrespective of whether they involved social (e.g., public speaking), cognitive (e.g., mental arithmetic), or experiential (e.g., parachute jumping) forms of stressful experience.

presents the meta-analysis of brief naturalistic stressors for medically healthy adults. The vast majority of these stressors (k = 60; 95.2%) involved students facing academic examinations. In contrast to the acute time-limited stressors, examination stress did not markedly affect the number or percentage of cells in peripheral blood. Instead, the largest effects were on functional parameters, particularly changes in cytokine production that indicate a shift away from cellular immunity (Th1) and toward humoral immunity (Th2). Brief stressors reliably changed the profile of cytokine production via a decrease in a Th1-type cytokine, IFN (r = .30), which stimulates natural and cellular immune functions, and increases in the Th2-type cytokines IL-6 (r = .26), which stimulates natural and humoral immune functions, and IL-10 (r = .41), which inhibits Th1 cytokine production. Note that IFN and IL-6 share the property of stimulating natural immunity but differentially stimulate cytotoxic versus inflammatory effector mechanisms. Their dissociation after brief naturalistic stress indicates differential effects between Th1 and Th2 responses rather than natural and specific responses.

Meta-Analysis of Immune Responses to Brief Naturalistic Stress in Healthy Participants

The functional assay data are consistent with this suggestion of suppression of cellular immunity via decreased Th1 cytokine production: The T cell proliferative response significantly decreased with brief stressors (r = .19 to .32), as did natural killer cell cytotoxicity (r = .11). Increased antibody production to latent virus, particularly Epstein-Barr virus (r = .20), is also consistent with suppression of cellular immunity, enhancement of humoral immunity, or both.

There was also evidence that age contributed to vulnerability to stress-related immune change during brief naturalistic stressors, even within a limited range of relatively young ages. When we examined whether effect sizes varied according to demographic characteristics of the sample, sex ratio did not show a consistent pattern of relations with immune processes. However, the mean age of the sample was strongly related to study effect size. To the extent that a study enrolled participants of older ages, it was likely to observe more pronounced decreases in natural killer cell cytotoxicity (r = .58, p = .04; k = 14), T lymphocyte proliferation to the mitogens PHA (r = .58, p = .04; k = 13) and ConA (r = .31, p = .38; k = 9), and production of the cytokine IFN (r = .63, p = .09; k = 8) in response to brief naturalistic stress. The strength of these findings is particularly surprising given the narrow range of ages found in studies of brief natural stress; the mean participant age in this literature ranged from 15.7 to 35.0 years.

We also calculated effect sizes for three studies examining the effects of examination stress on individuals with asthma (see ). These three studies, all emanating from a team of investigators at the University of WisconsinMadison, found that stress reliably increased superoxide release (r = .20 to .37) and decreased natural killer cell cytotoxicity (r = .33). Because natural killer cells are stimulated by Th1 cytokines, this change is consistent with a Th1-to-Th2 shift. However, stress also reliably increased T cell proliferation to PHA (r = .32), which is not consistent with such a shift. The generally larger effect sizes are consistent with the idea that individuals with immunologically mediated disease are more susceptible to stress-related immune dysregulation, but the reversed sign for T cell proliferation also indicates that that pattern of dysregulation may also be more disorganized. That is, the organized pattern of suppression of Th1 but not Th2 immune responses in healthy individuals undergoing brief stressors may reflect regulation in the healthy immune system. In contrast, the lack of regulation in a diseased immune system may lead to more chaotic changes during stressors.

Meta-Analysis of Immune Responses to Brief Naturalistic Stress in Participants With Asthma

The meta-analysis of stressful event sequences is presented in . With the exception of significant increases in the number of circulating natural killer cells and the number of antibodies to the latent Epstein-Barr virus, the findings indicate that stressful event sequences are not associated with reliable immune changes. For many immune outcomes, however, significant heterogeneity statistics are evident. Studies of healthy adults generally fell into two categories that yielded disparate patterns of immune findings. The largest group of studies focused on the death of a spouse as a stressor and, as such, used samples consisting primarily of older women. Collectively, these studies found that losing a spouse was associated with a reliable decline in natural killer cell cytotoxicity (r = .23, p = .01; k = 6) but not with alterations in stimulated-lymphocyte proliferation by the mitogens ConA (r = .04, p = .45; k = 4), PHA (r = .01, p = .93; k = 7), or PWM (r = .08, p = .76; k = 3) or with changes in the number of T-helper lymphocytes (r = .07, p = .52; k = 6) or T-cytotoxic lymphocytes (r = .13, p = .45; k = 5) in peripheral blood. The next largest group of studies in this area examined immune responses to disasters, which may have different neuroendocrine consequences than loss; whereas loss is generally associated with increases in cortisol, trauma may be associated with decreases in cortisol (Yehuda, 2001; Yehuda, McFarlane, & Shalev, 1998). Natural disaster samples tended to focus on middle-aged adults of both sexes who were direct victims of the disaster, rescue workers at the scene, or personnel at nearby medical centers. There were medium-size effects suggesting increases in natural killer cell cytotoxicity (r = .25, p = .53; k = 4) and stimulated-lymphocyte proliferation by the mitogen PHA (r = .26, p = .33; k = 2), as well as decreases in the number of T-helper lymphocytes (r = .20, p = .43; k = 2) and T-cytotoxic lymphocytes (r = .23, p = .55; k = 2) in the circulation. However, none of them was statistically significant because of the small number of studies involved, and therefore these effects should be considered suggestive but not reliable.

Meta-Analysis of Immune Responses to Stressful Event Sequences in Healthy Participants

An additional group of studies in this area examined immune responses to a positive initial biopsy for breast cancer in primarily middle-aged female participants before and after the procedure. The three studies of this nature did not yield a consistent pattern of relations with any of the immune outcomes.

In summary, stressful event sequences did not elicit a robust pattern of immune changes when considered as a whole. When these sequences are broken down into categories reflecting the stressors nature, the meta-analysis yields evidence of declines in natural immune response following the loss of a spouse, nonsignificant increases in natural and specific immune responses following exposure to natural disaster, and no immune alterations with breast biopsy. Unfortunately, we cannot determine whether these disparate patterns of immune response are attributable to features of the stressors, demographic or medical characteristics of the participants, or some interaction between these factors.

Chronic stressors included dementia caregiving, living with a handicap, and unemployment. Like other nonacute stressors, they did not have any systematic relationship with enumerative measures of the immune system. They did, however, have negative effects on almost all functional measures of the immune system (see ). Both natural and specific immunity were negatively affected, as were Th1 (e.g., T cell proliferative responses) and Th2 (e.g., antibody to influenza vaccine) parameters. The only nonsignificant change was for antibody to latent virus; this effect size was substantial (r = .44), but there was also substantial heterogeneity. Further analyses showed that demographics did not moderate this effect: Immune responses to chronic stressors were equally strong across the age spectrum as well as across sex.

Meta-Analysis of Immune Responses to Chronic Stress in Healthy Participants

Distant stressors were traumatic events such as combat exposure or abuse occurring years prior to immune assessment. The meta-analytic results for distant stressors appear in . The only immune outcome that has been examined regularly in this literature is natural killer cell cytotoxicity, and it is not reliably altered in persons who report a distant traumatic experience.

Meta-Analysis of Immune Responses to Distant Stressors and Posttraumatic Stress Disorder in Healthy Participants

Most of the studies in this area examined whether immune responses varied as a function of the number of life events a person endorsed on a standard checklist, a persons rating of the impact of those events, or both. As illustrates, this methodology yielded little in the way of significant outcomes in healthy participants. To determine whether vulnerability to life events might vary across the life span, we divided studies into two categories on the basis of a natural break in the age distribution. These analyses provided evidence that older adults are especially vulnerable to life-eventinduced immune change. In studies that used samples of adults who had a mean age above 55, life events were associated with reliable declines in lymphocyte-proliferative responses to PHA (r = .40, p = .05; k = 2) and natural killer cell cytotoxicity (r = .59, p = .001; k = 2). These effects were much weaker in studies with a mean age below 55: Life events were not associated with proliferative responses to PHA (r = .22, p = .24; k = 2), and showed a reliable but modest relationship with natural killer cell cytotoxicity (r = .10, p = .03; k = 8). The differences in effect size between older and younger adults were statistically significant for natural killer cell cytotoxicity ( p < .001) but not PHA-induced proliferation ( p <.15). None of the other moderators we examinedsex ratio, kind of life event assessed (daily hassle vs. major event), or the method used to do so (checklist vs. interview)was related to immune outcomes.

Meta-Analysis of Immune Responses to Major and Minor Life Events of Unknown Duration in Healthy Participants

presents the relationship between life events and immune parameters in participants with HIV/AIDS. The presence of life events was associated with a significant reduction in the number of natural killer cells and a marginal reduction in the number of T-cytotoxic lymphocytes. It is unrelated to the number of T-helper lymphocytes, the percentage of T-cytotoxic lymphocytes, and the T-helper:T-cytotoxic ratio, all of which are recognized indicators of disease progression for patients with HIV/AIDS.

Meta-Analysis of Immune Responses to Major and Minor Life Events of Unknown Duration in Participants With HIV/AIDS

We have already proposed that immunological disease diminishes the resilience and self-regulation of the immune system, making it more vulnerable to stress-related disruption, and this may be the case in HIV-infected versus healthy populations. However, studies of HIV-infected populations also utilized more refined measures of life events (interviews that factor in biographical context) than did studies of healthy populations (typically, checklist measures). Unfortunately, we cannot differentiate between these explanations on the basis of the available data.

The meta-analysis of stress appraisals and intrusive thoughts is displayed in . These studies generally enrolled large populations of adults who were not experiencing any specific form of stress and examined whether their immune responses varied according to stress appraisals and/or intrusive thoughts. This methodology was unsuccessful at documenting immune changes related to stress. Because of the small number of studies in this category, moderator analyses could not be performed.

Meta-Analysis of Immune Responses to Global Stress Appraisals in Healthy Participants

The meta-analysis results shown in address a similar question with regard to persons who are in the midst of a specific event sequence or a chronic stressor. To the extent that they appraise their lives as stressful or report the occurrence of intrusive thoughts, these individuals exhibit a significant reduction in natural killer cell cytotoxicity. Although this effect does not extend to the number of T-helper and T-cytotoxic lymphocytes in the circulation, it suggests that a persons subjective representation of a stressor may be a determinant of its impact on the immune response.

Meta-Analysis of Immune Responses to Stress Appraisals and Intrusive Thoughts Within Healthy Stressed Populations

The large number of effect sizes generated by the meta-analysis raises the possibility of Type I error. One strategy for evaluating this concern involves dividing the number of significant findings in a meta-analysis by the total number of analyses conducted. When we performed this calculation, a value of 25.6% emerged, suggesting that more than one fourth of the analyses yielded reliable findings. This exceeds the 5% value at which investigators typically become concerned about Type I error rates and gives us confidence that the meta-analytic findings presented here are robust.

A second concern arises from the publication bias toward positive findings, which could skew meta-analytic results toward larger effect sizes. Fortunately, recent advances in meta-analysis enable one to evaluate the extent of this publication bias by using graphical techniques. A funnel plot can be drawn in which effect sizes are plotted against sample sizes for any group of studies. Because most studies in any given area have small sample sizes and therefore tend to yield more variable findings, the plot should end up looking like a funnel, with a narrow top and a wide bottom. If there is a bias against negative findings in an area, the plot is shifted toward positive values or a chunk of it will be missing entirely.

We drew funnel plots for all of the immune outcomes in the meta-analysis for which there were a sufficient number of observations. Although not all of them yielded perfect funnels, there was no systematic evidence of publication bias. Space limitations prevent us from including all plots; however, displays three plots that are prototypical of those we drew. As is evident from the data in the figure, psychoneuroimmunology researchers seem to be reporting positive and negative findingsand not hiding unfavorable outcomes when they do emerge. Thus, we do not have any major concerns about publication bias leading this meta-analysis to dramatically overestimate effect sizes.

Funnel plots depicting relationship between effect size and sample size. PHA = phytohemagglutinin.

The immune system, once thought to be autonomous, is now known to respond to signals from many other systems in the body, particularly the nervous system and the endocrine system. As a consequence, environmental events to which the nervous system and endocrine system respond can also elicit responses from the immune system. The results of meta-analysis of the hundreds of research reports generated by this hypothesis indicate that stressful events reliably associate with changes in the immune system and that characteristics of those events are important in determining the kind of change that occurs.

Selyes (1975) seminal findings suggested that stress globally suppressed the immune system and provided the first model for how stress and immunity are related. This model has recently been challenged by views that relations between stress and the immune system should be adaptive, at least within the context of fight-or-flight stressors, and an even newer focus on the balance between cellular and humoral immunity. The present meta-analytic results support three of these models. Depending on the time frame, stressors triggered adaptive upregulation of natural immunity and suppression of specific immunity (acute time-limited), cytokine shift (brief naturalistic), or global immunosuppression (chronic).

When stressors were acute and time-limitedthat is, they generally followed the temporal parameters of fight-or-flight stressorsthere was evidence for adaptive redistribution of cells and preparation of the natural immune system for possible infection, injury, or both. In evolution, stressor-related changes in the immune system that prepared the organisms for infections resulting from bites, puncture wounds, scrapes, or other challenges to the integrity of the skin and blood could be selected for. This process would be most adaptive when it was also efficient and did not divert excess energy from fight-or-flight behavior. Indeed, changes in the immune system following acute stress conformed to this pattern of efficiency and energy conservation. Acute stress upregu-lated parameters of natural immunity, the branch of the immune system in which most changes occurred, which requires only minimal time and energy investment to act against invaders and is also subject to the fewest inhibitory constraints on acting quickly (Dopp et al., 2000; Sapolsky, 1998). In contrast, energy may actually be directed away from the specific immune response, as indexed by the decrease in the proliferative response. The specific immune response in general and proliferation in particular demand time and energy; therefore, this decrease might indicate a redirection away from this function. Similar redirection occurs during fight-or-flight stressors with regard to other nonessential, future-oriented processes such as digestion and reproduction. As stressors became more chronic, the potential adaptiveness of the immune changes decreased. The effect of brief stressors such as examinations was to change the potency of different arms of specific immunityspecifically, to switch away from cellular (Th1) immunity and toward humoral (Th2) immunity.

The stressful event sequences tended to fall into two substantive groups: bereavement and trauma. Bereavement was associated with decreased natural killer cell cytotoxicity. Trauma was associated with nonsignificantly increased cytotoxicity and increased proliferation but decreased numbers of T cells in peripheral blood. The different results for loss and trauma mirror neuroendocrine effects of these two types of adverse events. Lossmaternal separation in nonhuman animals and bereavement in humansis commonly associated with increased cortisol production (Irwin, Daniels, Risch, Bloom, & Weiner, 1988; Laudenslager, 1988; McCleery, Bhagwagar, Smith, Goodwin, & Cowen, 2000). In contrast, trauma and posttraumatic stress disorder are commonly associated with decreased cortisol production (see Yehuda, 2001; Yehuda et al., 1998, for reviews). To the degree that cortisol suppresses immune function such as natural killer cell cytotoxicity, these results have the potential to explain the different effects of loss and trauma event sequences.

The most chronic stressors were associated with the most global immunosuppression, as they were associated with reliable decreases in almost all functional immune measures examined. Increasing stressor duration, therefore, resulted in a shift from potentially adaptive changes to potentially detrimental changes, initially in cellular immunity and then in immune function more broadly. It is important to recognize that although the effects of chronic stressors may be due to their duration, the most chronic stressors were associated with changes in identity or social roles (e.g., acquiring the role of caregiver or refugee or losing the role of employee). These chronic stressors may also be more persistent, that is, constantly rather than intermittently present. Finally, chronic stressors may be less controllable and afford less hope for control in the future. These qualities could contribute to the severity of the stressor in terms of both its psychological and physiological impact.

Increasing stressor chronicity also impacted the type of parameter in which changes were seen. Compared with the natural immune system, the specific immune system is time and energy intensive and as such is expected to be invoked only when circumstances (either a stressor or an infection; cf. Maier & Watkins, 1998) persist for a longer period of time. Affected immune domainsnatural versus specificwere consistent with the duration of the stressorsacute versus chronic. Furthermore, changing immune responses via redistribution of cells can happen much faster than changes via the function of cells. The time frames of the stressor and the immune domain were also consistent; acute stress affected primarily enumerative measures, whereas stressors of longer duration affected primarily functional measures.

The results of these analyses suggest that the dichotomization of the immune system into natural and specific categories and, within specific immunity, into cellular and humoral measures, is a useful starting point with regard to understanding the effects of stressors. Categorizing an immune response is a difficult process, as each immune response is highly redundant and includes natural, specific, cellular, and humoral immune responses acting together. Given this redundancy, the differential results within these theoretical divisions were remarkably, albeit not totally, consistent. As further immunological research defines these divisions more subtly, the results with regard to stressors may become even clearer. However, the present results suggest that the categories used here are meaningful.

The results of this meta-analysis reflect the theoretical and empirical progress of this literature over the past 4 decades. Increased differentiation in the quality of stressors and the immunological parameters investigated have allowed complex models to be tested. In contrast, previous meta-analyses were bound by a small number of more homogenous studies. Herbert and Cohen (1993) reported on 36 studies published between 1977 and 1991, finding broadly immunosuppressive effects of stress. Zorrilla et al. (2001) reported on 82 studies published between 1980 and 1996, finding potentially adaptive effects of acute stressors in addition to evidence for immunosuppression with longer stressors. It is important to note that meta-analytic findings are bound by the models tested in the literature. As more complex models are tested, more complex relationships emerge in meta-analysis. We next consider some such areas of complexity that should be considered in future psychoneuroimmunology research.

The meta-analytic results indicate that organismic variables such as age and disease status moderate vulnerability to stress-related decreases in functional immune measures. Both aging and HIV are associated with immune senescence and loss of responsiveness (Effros et al., 1994; Effros & Pawelec, 1997), and both are also associated with disruption of neuroendocrine inputs to the immune system (Kumar et al., 2002; Madden, Thyagarajan, & Felten, 1998). The loss of self-regulation in disease and aging likely makes affected people more susceptible to negative immunological effects of stress. Finally, the meta-analysis did not reveal effects of sex on immune responses to stressors. However, these comparisons simply correlated the sex ratio of the studies with effect sizes. Grouping data by sex would afford a more powerful comparison, but few studies organized their data that way. Gender may moderate the effects of stress on immunity by virtue of the effects of sex hormones on immunity; generally, men are considered to be more biologically vulnerable (Maes, 1999), and they may be more psychosocially vulnerable (e.g.,Scanlan, Vitaliano, Ochs, Savage, & Borson, 1998).

It seems likely to us that individual differences in subjective experience also make a substantive contribution to explaining this phenomenon. Studies have convincingly demonstrated that peoples cardiovascular and neuroendocrine responses to stressful experience are dependent on their appraisals of the situation and the presence of intrusive thoughts about it (Baum et al., 1993; Frankenhauser, 1975; Tomaka et al., 1997). Although the same logic should apply to peoples immune responses to stressful experience, few of the studies in this area have included measures of subjective experience, and those reports were limited by methodological issues such as aggregation across heterogeneous stressors. As a consequence, measures of subjective experience were not significantly associated with immune parameters in healthy research participants, with the exception of a modest (r = .10) relationship between intrusive thoughts and natural killer cell cytotoxicity. Psychological variables such as personality and emotion can give rise to individual differences in psychological and concomitant immunological responses to stress. Optimism and coping, for example, moderated immunological responses to stressors in several studies (e.g., Barger et al., 2000; Bosch et al., 2001; Cruess et al., 2000; Segerstrom, 2001; Stowell, Kiecolt-Glaser, & Glaser, 2001).

Virtually nothing is known about the psychological pathways linking stressors with the immune system. Many theorists have argued that affect is a final common pathway for stressors (e.g., S. Cohen, Kessler, & Underwood, 1995; Miller & Cohen, 2001), yet studies have enjoyed limited success in attempting to explain peoples immune responses to life experiences on the basis of their emotional states alone (Bower et al., 1998; Cole, Kemeny, Taylor, Visscher, & Fahey, 1996; Miller, Dopp, Myers, Stevens, & Fahey, 1999; Segerstrom, Taylor, Kemeny, & Fahey, 1998). Furthermore, many studies have focused on the immune effects of emotional valence (e.g., unhappy vs. happy; Futterman, Kemeny, Shapiro, & Fahey, 1994), but the immune system may be even more closely linked to emotional arousal (e.g., stimulated vs. still), especially during acute stressors (S. Cohen et al., 2000). Finally, it is possible that emotion will prove to be relatively unimportant and that other mental processes such as motivational states or cognitive appraisals will prove to be the critical psychological mechanisms linking stress and the immune system (cf. Maier, Waldstein, & Synowski, 2003).

In terms of biological mechanisms, the field is further along, but much remains to be learned. A series of studies in the mid-1990s was able to show via beta-adrenergic blockade that activation of the sympathetic nervous system was responsible for the immune system effects of acute stressors (Bachen et al., 1995; Benschop, Nieuwenhuis, et al., 1994). Apart from these findings, however, little is known about biological mechanisms, especially with regard to more enduring stressors that occur in the real world. Studies that have attempted to identify hormonal pathways linking stressors and the immune system have enjoyed limited success, perhaps because they have utilized snapshot assessments of hormones circulating in blood. Future studies can maximize their chances of identifying relevant mediators by utilizing more integrated measures of hormonal output, such as 24-hr urine collections or diurnal profiles generated through saliva collections spaced throughout the day (Baum & Grunberg, 1995; Stone et al., 2001).

Future studies could also benefit from a greater emphasis on behavior as a potential mechanism. This strategy has proven useful in studies of clinically depressed patients, in which decreased physical activity and psychomotor retardation (Cover & Irwin, 1994; Miller, Cohen, & Herbert, 1999), increased body mass (Miller, Stetler, Carney, Freedland, & Banks, 2002), disturbed sleep (Cover & Irwin, 1994; Irwin, Smith, & Gillin, 1992), and cigarette smoking (Jung & Irwin, 1999) have been shown to explain some of the immune dysregulation evident in this population. There is already preliminary evidence, for instance, that sleep loss might be responsible for some of the immune system changes that accompany stressors (Hall et al., 1998; Ironson et al., 1997).

The most pressing question that future research needs to address is the extent to which stressor-induced changes in the immune system have meaningful implications for disease susceptibility in otherwise healthy humans. In the 30 years since work in the field of psychoneuroimmunology began, studies have convincingly established that stressful experiences alter features of the immune response as well as confer vulnerability to adverse medical outcomes that are either mediated by or resisted by the immune system. However, with the exception of recent work on upper respiratory infection (S. Cohen, Doyle, & Skoner, 1999), studies have not yet tied these disparate strands of work together nor determined whether immune system changes are the mechanism through which stressors increase susceptibility to disease onset. In contrast, studies of vulnerable populations such as people with HIV have shown changes in immunity to predict disease progression (Bower et al., 1998).

To test an effect of this nature, researchers need to build clinical outcome assessments into study designs where appropriate. For example, chronic stressors reliably diminish the immune systems capacity to produce antibodies following routine influenza vaccinations (see ). Yet as far as we are aware, none of these studies has tracked illness to explore whether stress-related disparities in vaccine response might be sufficient to heighten susceptibility to clinical infection with influenza. Cytokine expression represents a relatively new and promising example of an avenue for research linking stress, immune change, and disease. For example, chronic stress may elicit prolonged secretion of cortisol, to which white blood cells mount a counterregulatory response by downregulating their cortisol receptors. This downregulation, in turn, reduces the cells capacity to respond to anti-inflammatory signals and allows cytokine-mediated inflammatory processes to flourish (Miller, Cohen, & Ritchey, 2002). Stress therefore might contribute to the course of diseases involving excessive nonspecific inflammation (e.g., multiple sclerosis, rheumatoid arthritis, coronary heart disease) and thereby increase risk for excess morbidity and mortality (Ershler & Keller, 2000; Papanicoloaou et al., 1998; Rozanski, Blumenthal, & Kaplan, 1999). Another example of the importance of cytokines to clinical pathology is in asthma and allergy, in which emerging evidence implicates excess Th2 cytokine secretion in the exacerbation of these diseases (Busse & Lemanske, 2001; Luster, 1998).

Sapolsky (1998) wrote,

Stress-related disease emerges, predominantly, out of the fact that we so often activate a physiological system that has evolved for responding to acute physical emergencies, but we turn it on for months on end, worrying about mortgages, relationships, and promotions. (p. 7)

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Psychological Stress and the Human Immune System: A Meta ...

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Glossary Index | womenshealth.gov

Thursday, August 4th, 2016

Find your glossary term by first letter:

a form of complementary and alternative medicine that involves inserting thin needles through the skin at specific points on the body to control pain and other symptoms.

written instructions letting others know the type of care you want if you are seriously ill or dying. These include a living will and health care power of attorney.

disorders that involve an immune response in the body. Allergies are reactions to allergens such as plant pollen, other grasses and weeds, certain foods, rubber latex, insect bites, or certain drugs.

tiny glands in the breast that produce milk.

a brain disease that cripples the brain's nerve cells over time and destroys memory and learning. It usually starts in late middle age or old age and gets worse over time. Symptoms include loss of memory, confusion, problems in thinking, and changes in language, behavior, and personality.

clear, slightly yellowish liquid that surrounds the unborn baby (fetus) during pregnancy. It is contained in the amniotic sac.

when the amount of red blood cells or hemoglobin (the substance in the blood that carries oxygen to organs) becomes reduced, causing fatigue that can be severe.

the use of medicine to prevent the feeling of pain or another sensation during surgery or other procedures that might be painful.

a thin or weak spot in an artery that balloons out and can burst.

anticancer drugs that can stop or slow down biochemical reactions in cells.

drugs that inhibit the ability of HIV or other types of retroviruses to multiply in the body.

the body opening from which stool passes from the lower end of the intestine and out of the body.

a form of complementary and alternative medicine in which the scent of essential oils from flowers, herbs, and trees is inhaled to promote health and well-being.

blood vessels that carry oxygen and blood to the heart, brain and other parts of the body.

technology that involves procedures that handle a woman's eggs and a man's sperm to help infertile couples conceive a child.

dry and itchy skin, caused by certain diseases, irritating substances, allergies, or a persons genetic makeup.

a medical condition in kids and adults that makes it hard to sit still, pay attention, and focus on certain tasks.

a condition in which abnormal breast cells are found in either the breast lobules (atypical lobular hyperplasia) or the breast ducts (atypical ductal hyperplasia). Atypical hyperplasia is not cancer. But having it increases breast cancer risk.

blood proteins made by the body's immune system that are meant to neutralize and destroy germs or other foreign substances but instead attack healthy cells of the body.

an immune response by the body against one of its own tissues, cells, or molecules.

disease caused by an immune response against foreign substances in the tissues of one's own body.

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microorganisms that can cause infections.

noncancerous

a type of medication that reduces nerve impulses to the heart and blood vessels. This makes the heart beat slower and with less force. Blood pressure drops and the heart works less hard.

a brown liquid made by the liver. It contains some substances that break up fat for digestion, while other substances are waste products.

when the hemoglobin in a person's blood breaks down, causing a yellowing of the skin and whites of the eyes. It is a temporary condition in newborn infants.

an eating disorder caused by a person being unable to control the need to overeat.

having to do with, or related to, living things.

removal of a small piece of tissue for testing or examination under a microscope.

medical illness that causes unusual shifts in mood, energy, and activity levels. It is also known as manic-depressive illness. A person with bipolar disorder may switch from feeling extremely joyful or excited to feeling extremely sad and hopeless very quickly.

a special place for women to give birth. They have all the required equipment for birthing, but are specially designed for a woman, her partner, and family. Birth centers may be free standing (separate from a hospital) or located within a hospital.

the organ in the human body that stores urine. It is found in the lower part of the abdomen.

fluid in the body made up of plasma, red and white blood cells, and platelets. Blood carries oxygen and nutrients to and waste materials away from all body tissues. In the breast, blood nourishes the breast tissue and provides nutrients needed for milk production.

blood pressure is the force of blood against the walls of arteries. Blood pressure is noted as two numbersthe systolic pressure (as the heart beats) over the diastolic pressure (as the heart relaxes between beats). The numbers are written one above or before the other, with the systolic number on top and the diastolic number on the bottom. For example, a blood pressure reading of 120/80 mmHg (millimeters of mercury) is called 120 over 80.

the transfer of blood or blood products from one person (donor) into another person's bloodstream (recipient). Most times, it is done to replace blood cells or blood products lost through severe bleeding. Blood can be given from two sources, your own blood (autologous blood) or from someone else (donor blood).

how a person feels about how she or he looks.

a measure of body fat based on a person's height and weight.

also known as the intestine, which is a long tube-like organ in the human body that completes digestion or the breaking down of food. The small bowel is the small intestine and the large bowel is the large intestine.

inflammation of the main air passages (bronchi) to your lungs. It causes cough, shortness of breath, and chest tightness.

an eating disorder caused by a person consuming an extreme amount of food all at once followed by self-induced vomiting or other purging.

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a unit of energy-producing potential in food.

a term for diseases in which abnormal cells in the body divide without control. Cancer cells can invade nearby tissues and can spread to other parts of the body through the blood and lymphatic system, which is a network of tissues that clears infections and keeps body fluids in balance.

compounds such as sugars and starches that occur in food and are broken down to release energy in the body.

disease of the heart and blood vessels.

a sudden loss of motor tone and strength.

cloudy or thick areas in the lens of the eye.

disease of the blood vessels in the brain.

procedure where the baby is delivered through an abdominal incision. Also called cesarean delivery or cesarean birth.

treatment with anticancer drugs.

an alternative medical system that takes a different approach from standard medicine in treating health problems. The goal of chiropractic therapy is to normalize this relationship between your body's structure (mainly the spine) and its function. Chiropractic professionals use a type of hands-on therapy called spinal manipulation or adjustment.

If necessary this test is performed between 10 and 12 weeks of pregnancy and can indicate the same chromosomal abnormalities and genetic disorders as amniocentesis can. It also can detect the baby's sex and risk of spina bifida.

long-lasting, such as a chronic illness or chronic disease.

a complex disorder characterized by extreme fatigue that lasts six months or longer, and does not improve with rest or is worsened by physical or mental activity. Other symptoms can include weakness, muscle pain, impaired memory and/or mental concentration, and insomnia. The cause is unknown.

birth defects that affect the upper lip and the hard and soft palates of the mouth. Features range from a small notch in the lip to a complete fissure or groove, extending into the roof of the month and nose. These features may occur separately or together.

an external female sex organ located near the top of the inner labia of the vagina. The clitoris is very sensitive to the touch, and for most women it is a center of sexual pleasure.

to force someone to do something that they do not want to do.

a diagnostic procedure in which a flexible tube with a light source in inserted into the colon (large intestine or large bowel) through the anus to view all sections of the colon for abnormalities.

thick, yellowish fluid secreted from breast during pregnancy, and the first few days after childbirth before the onset of mature breast milk. Also called first milk, it provides nutrients and protection against infectious diseases.

abnormalities of the heart's structure and function caused by abnormal or disordered heart development before birth.

a type of body tissue that supports other tissues and binds them together. Connective tissue provides support in the breast.

infrequent or hard stools or difficulty passing stools.

transmitted by direct or indirect contact.

usually has a master's degree in Counseling and has completed a supervised internship.

an ongoing condition that causes inflammation of the digestive tract, also called the GI tract. It can affect any part of the GI tract from the mouth to the anus. It often affects the lower part of the small intestine, causing pain and diarrhea.

one of the most common serious genetic (inherited) diseases. One out of every 400 couples is at risk for having children with CF. CF causes the body to make abnormal secretions leading to mucous build-up. CF mucous build-up can impair organs such as the pancreas, the intestine and the lungs.

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impairs the vitality and strength of a person.

medications that treat cough and stuffy nose by shrinking swollen membranes in the nose and making it easier to breath.

excessive loss of body water that the body needs to carry on normal functions at an optimal level. Signs include increasing thirst, dry mouth, weakness or lightheadedness (particularly if worse on standing), and a darkening of the urine or a decrease in urination.

when a person believes something that is not true and that person keeps the belief even though there is strong evidence against it. Delusions can be the result of brain injury or mental illness.

a square, thin piece of latex that can be placed over the anus or the vagina before oral sex.

term used to describe an emotional state involving sadness, lack of energy and low self-esteem.

medical treatment used when kidneys fail. Special equipment filters the blood to rid the body of harmful wastes, salt, and extra water.

tube through which food passes and is digested, and wastes are eliminated. The digestive tract runs from the mouth to the anus and includes the esophagus, stomach, and intestines.

a physical or mental impairment that interferes with or prevents normal achievement in a particular function.

a lab test in which a patient's DNA is tested. DNA is a molecule that has a person's genetic information and is found in every cell in a person's body.

Down syndrome is the most frequent genetic cause for mild to moderate mental retardation and related medical problems. It is caused by a chromosomal abnormality. For an unknown reason, a change in cell growth results in 47 instead of the usual 46 chromosomes. This extra chromosome changes the orderly development of the body and brain.

a condition in which abnormal cells are found in the lining of breast ducts. These cells have not spread outside the duct to the surrounding breast tissue. DCIS is not cancer. But some cases of DCIS become breast cancer over time, so its important to get treatment for DCIS.

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an external, noninvasive test that records the electrical activity of the heart.

a period during pregnancy where the baby has rapid growth, and the main external features begin to take form.

a condition caused by damage to the air sacs in the lungs. This damage keeps the body from getting enough oxygen. Symptoms include trouble breathing, cough, and trouble exercising for more than brief periods. Emphysema is usually caused by smoking.

a diagnostic procedure in which a thin, flexible tube is introduced through the mouth or rectum to view parts of the digestive tract.

during labor a woman may be offered an epidural, where a needle is inserted into the epidural space at the end of the spine, to numb the lower body and reduce pain. This allows a woman to have more energy and strength for the end stage of labor, when it is time to push the baby out of the birth canal.

inability to achieve and keep a penile erection.

tube that connects the throat with the stomach.

when someone exposes him/herself in public

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a federal regulation that allows eligible employees to take up to 12 work weeks of unpaid leave during any 12 month period for the serious health condition of the employee, parent, spouse or child, or for pregnancy or care of a newborn child, or for adoption or foster care of a child.

a rare, inherited blood disorder that leads to bone marrow failure. FA causes your bone marrow to stop making enough new blood cells for your body to work normally. The risk for some cancers is much greater for people with FA.

a source of energy used by the body to make substances it needs. Fat helps your body absorb certain vitamins from food. Some fats are better for your health than others. To help prevent heart disease and stroke, most of the fats you eat should be monounsaturated (mon-oh-uhn-SACH-uh-ray-tid) and polyunsaturated (pol-ee-uhn-SACH-uh-ray-tid) fats.

a feeling of lack of energy, weariness or tiredness.

a barrier form of birth control that is worn by the woman inside her vagina. It is made of thin, flexible, manmade rubber. It keeps sperm from getting into her body.

a term used to describe the full range of harmful effects that can occur when a fetus is exposed to alcohol.

body temperature is raised above normal and is usually a sign of infection or illness.

a disorder that causes aches and pain all over the body, and involves tender points on specific places on the neck, shoulders, back, hips, arms, and legs that hurt when pressure is put on them.

each month, an egg develops inside the ovary in a fluid filled pocket called a follicle. This follicle releases the egg into the fallopian tube.

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Glossary Index | womenshealth.gov

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A Comprehensive Guide to Understanding the Immune System

Thursday, August 4th, 2016

Mary Shomon

Acquired immunodeficiency syndrome (AIDS):A life-threatening disease caused by a virus and characterized by breakdown of the body's immune defenses.

Active immunity:Immunity produced by the body in response to stimulation by a disease-causing organism or a vaccine.

Agammaglobulinemia:An almost total lack of immunoglobulins, or antibodies.

Allergen:Any substance that causes an allergy.

Allergy:An inappropriate and harmful response of the immune system to normally harmless substances.

Anaphylactic shock:A life-threatening allergic reaction characterized by a swelling of body tissues including the throat, difficulty in breathing, and a sudden fall in blood pressure.

Anergy:A state of unresponsiveness, induced when the T cell's antigen receptor is stimulated, that effectively freezes T cell responses pending a "second signal" from the antigen-presenting cell (co-stimulation).

Antibody:A soluble protein molecule produced and secreted by B cells in response to an antigen, which is capable of binding to that specific antigen.

Antibody-dependent cell-mediated cytotoxicity (ADCC):An immune response in which antibody, by coating target cells, makes them vulnerable to attack by immune cells.

Antigen:Any substance that, when introduced into the body, is recognized by the immune system.

Antigen-presenting cells:B cells, cells of the monocyte lineage (including macrophages as well as dendritic cells), and various other body cells that "present" antigen in a form that T cells can recognize.

Antinuclear antibody (ANA):An autoantibody directed against a substance in the cell's nucleus.

Antiserum:Serum that contains antibodies.

Antitoxins:Antibodies that interlock with and inactivate toxins produced by certain bacteria.

Appendix:Lymphoid organ in the intestine.

Attenuated:Weakened; no longer infectious.

Autoantibody:An antibody that reacts against a person's own tissue.

Autoimmune disease:A disease that results when the immune system mistakenly attacks the body's own tissues. Rheumatoid arthritis and systemic lupus erythematosus are autoimmune diseases.

Bacterium:A microscopic organism composed of a single cell. Many but no all bacteria cause disease.

Basophil:A white blood cell that contributes to inflammatory reactions. Along with mast cells, basophils are responsible for the symptoms of allergy.

B cells:Small white blood cells crucial to the immune defenses. Also known as B lymphocytes, they are derived from bone marrow and develop into plasma cells that are the source of antibodies.

Biological response modifiers:Substances, either natural or synthesized, that boost, direct, or restore normal immune defenses. BRMs include interferons, interleukins, thymus hormones, and monoclonal antibodies.

Biotechnology:The use of living organisms or their products to make or modify a substance. Biotechnology includes recombinant DNA techniques (genetic engineering) and hybridoma technology.

Bone marrow:Soft tissue located in the cavities of the bones. The bone marrow is the source of all blood cells.

Cellular immunity:Immune protection provided by the direct action of immune cells (as distinct from soluble molecules such as antibodies).

Chromosomes:Physical structures in the cell's nucleus that house the genes. Each human cell has 23 pairs of chromosomes.

Clone:(n.)A group of genetically identical cells or organisms descended from a single common ancestor; (v.) to reproduce multiple identical copies.

Complement:A complex series of blood proteins whose action "complements" the work of antibodies. Complement destroys bacteria, produces inflammation, and regulates immune reactions.

Complement cascade:A precise sequence of events usually triggered by an antigen-antibody complex, in which each component of the complement system is activated in turn.

Constant region:That part of an antibody's structure that is characteristic for each antibody class.

Co-Stimulation:The delivery of a second signal from an antigen-presenting cell to a T cell. The second signal rescues the activated T cell from anergy, allowing it to produce the lymphokines necessary for the growth of additional T cells.

Cytokines:Powerful chemical substances secreted by cells. Cytokines include lymphokines produced by lymphocytes and monokines produced by monocytes and macrophages.

Cytotoxic T cells:A subset of T lymphocytes that can kill body cells infected by viruses or transformed by cancer.

Dendritic cells:White blood cells found in the spleen and other lymphoid organs. Dendritic cells typically use threadlike tentacles to enmesh antigen, which they present to T cells.

DNA (deoxyribonucleic acid):Nucleic acid that is found in the cell nucleus and that is the carrier of genetic information.

Enzyme:A protein, produced by living cells, that promotes the chemical processes of life without itself being altered.

Eosinophil:A white blood cell that contains granules filled with chemicals damaging to parasites, and enzymes that damp down inflammatory reactions.

Epitope:A unique shape or marker carried on an antigen's surface, which triggers a corresponding antibody response.

Fungus:Member of a class of relatively primitive vegetable organism. Fungi include mushrooms, yeasts, rusts, molds, and smuts.

Gene:A unit of genetic material (DNA) that carries the directions a cell uses to perform a specific function, such as making a given protein.

Graft-versus-host disease (GVHD):A life-threatening reaction in which transplanted immunocompetent cells attack the tissues of the recipient.

Granulocytes:White blood cells filled with granules containing potent chemicals that allow the cells to digest microorganisms, or to produce inflammatory reactions. Neutrophils, eosinophils, and basophils are examples of granulocytes.

Helper T cells:A subset of T cells that typically carry the T4 marker and are essential for turning on antibody production, activating cytotoxic T cells, and initiating many other immune responses.

Hematopoiesis:The formation and development of blood cells, usually takes place in the bone marrow.

Histocompatibility testing:A method of matching the self antigens (HLA) on the tissues of a transplant donor with those of the recipient. The closer the match, the better the chance that the transplant will take.

HIV (human immunodeficiency virus):The virus that causes AIDS.

Human leukocyte antigens (HLA):Protein in markers of self used in histocompatibility testing. Some HLA types also correlate with certain autoimmune diseases.

Humoral immunity:Immune protection provided by soluble factors such as antibodies, which circulate in the body's fluids or "humors," primarily serum and lymph.

Hybridoma:A hybrid cell created by fusing a B lymphocyte with a long-lived neoplastic plasma cell, or a T lymphocyte with a lymphoma cell. A B-cell hybridoma secretes a single specific antibody.

Hypogammaglobulinemia:Abno rmally low levels of immunoglobulins.

Idiotypes:The unique and characteristic parts of an antibody's variable region, which can themselves serve as antigens.

Immune complex:A cluster of interlocking antigens and antibodies.

Immune response:The reactions of the immune system to foreign substances.

Immunoassay:A test using antibodies to identify and quantify substances. Often the antibody is linked to a marker such as a fluorescent molecule, a radioactive molecule, or an enzyme.

Immunocompetent:Capable of developing an immune response.

Immunoglobulins:A family of large protein molecules, also known as antibodies.

Immunosuppression:Reduction of the immune responses, for instance by giving drugs to prevent transplant rejection.

Immunotoxin:A monoclonal antibody linked to a natural toxin, a toxic drug, or a radioactive substance.

Inflammatory response:Redness, warmth, swelling, pain, and loss of function produced in response to infection, as the result of increased flood flow and an influx of immune cells and secretions.

Interleukins:A major group of lymphokines and monokines.

Kupffer cells:Specialized macrophages in the liver.

LAK cells:Lymphocytes transformed in the laboratory into lymphokine-activated killer cells, which attack tumor cells.

Langerhans cells:Dendritic cells in the skin that pick up antigen and transport it to lymph nodes.

Leukocytes:All white blood cells.

Lymph:A transparent, slightly yellow fluid that carries lymphocytes, bathes the body tissues, and drains into the lymphatic vessels.

Lymphatic vessels:A bodywide network of channels, similar to the blood vessels, which transport lymph to the immune organs and into the bloodstream.

Lymph nodes:Small bean-shaped organs of the immune system, distributed widely throughout the body and linked by lymphatic vessels. Lymph nodes are garrisons of B, T, and other immune cells.

Lymphocytes:Small white blood cells produced in the lymphoid organs and paramount in the immune defenses.

Lymphoid organs:The organs of the immune system, where lymphocytes develop and congregate. They include the bone marrow, thymus, lymph nodes, spleen, and various other clusters of lymphoid tissue. The blood vessels and lymphatic vessels can also be considered lymphoid organs.

Lymphokines:Powerful chemical substances secreted by lymphocytes. These soluble molecules help direct and regulate the immune responses.

Macrophage:A large and versatile immune cell that acts as a microbe-devouring phagocyte, an antigen-presenting cell, and an important source of immune secretions.

Major histocompatibility complex (MHC):A group of genes that controls several aspects of the immune response. MHC genes code for self markers on all body cells.

Mast cell:A granule-containing cell found in tissue. The contents of mast cells, along with those of basophils, are responsible for the symptoms of allergy.

Microbes:Minute living organisms, including bacteria, viruses, fungi and protozoa.

Microorganisms:Microscopic plants or animals.

Molecule:The smallest amount of a specific chemical substance that can exist alone. (The break a molecule down into its constituent atoms is to change its character. A molecule of water, for instance, reverts to oxygen and hydrogen.)

Monoclonal antibodies:Antibodies produced by a single cell or its identical progeny, specific for a given antigen. As a tool for binding to specific protein molecules, monoclonal antibodies are invaluable in research, medicine, and industry.

Monocyte:A large phagocytic white blood cell which, when it enters tissue, develops into a macrophage.

Monokines:Powerful chemical substances secreted by monocytes and macrophages. These soluble molecules help direct and regulate the immune responses.

Natural killer (NK) cells:Large granule-filled lymphocytes that take on tumor cells and infected body cells. They are known as "natural" killers because they attack without first having to recognize specific antigens.

Neutrophil:A white blood cell that is an abundant and important phagocyte.

Nucleic acids:Large, naturally occurring molecules composed of chemical building blocks known as nucleotides. There are two kinds of nucleic acids, DNA and RNA.

OKT3:A monoclonal antibody that targets mature T cells.

Opportunistic infection:An infection in an immunosuppressed person caused by an organism that does not usually trouble people with healthy immune systems.

Opsonize:To coat an organism with antibodies or a complement protein so as to make it palatable to phagocytes.

Organism:An individual living thing.

Parasite:A plant or animal that lives, grows and feeds on or within another living organism.

Passive immunity:Immunity resulting from the transfer of antibodies or antiserum produced by another individual.

Peyer's patches:A collection of lymphoid tissues in the intestinal tract.

Phagocytes:Large white blood cells that contribute to the immune defenses by ingesting microbes or other cells and foreign particles.

Plasma cells:Large antibody-producing cells that develop from B cells.

Platelets:Granule-containing cellular fragments critical for blood clotting and sealing off wounds. Platelets also contribute to the immune response.

Polymorphs:Short for polymorphonuclear leukocytes or granulocytes.

Proteins:Organic compounds made up of amino acids. Proteins are one of the major constituents of plant and animal cells.

Protozoa:A group of one-celled animals, a few of which cause human disease (including malaria and sleeping sickness).

Rheumatoid factor:An autoantibody found in the serum of most persons with rheumatoid arthritis.

RNA (ribonucleic acid):A nucleic acid that is found in the cytoplasm and also in the nucleus of some cells. One function of RNA is to direct the synthesis of proteins.

Scavenger cells:Any of a diverse group of cells that have the capacity to engulf and destroy foreign material, dead tissues, or other cells.

SCID mouse:A laboratory animal that, lacking an enzyme necessary to fashion an immune system of its own, can be turned into a model of the human immune system when injected with human cells or tissues.

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A Comprehensive Guide to Understanding the Immune System

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Immune system – New World Encyclopedia

Friday, October 23rd, 2015

The immune system is the system of specialized cells and organs that protects an organism from outside biological influences (though in a broad sense, almost every organ has a protective functionfor example, the tight seal of the skin or the acidic environment of the stomach).

When the immune system is functioning properly, it protects the body against bacteria and viral infections and destroys cancer cells and foreign substances. If the immune system weakens, its ability to defend the body also weakens, allowing pathogens (infectious agents), including viruses that cause common colds and flu, to survive and flourish in the body. Because the immune system also performs surveillance of tumor cells, immune suppression has been reported to increase the risk of certain types of cancer.

The complex coordination of the immune system is stunning. It is capable of recognizing millions of invaders and neutralizing their attacks, and yet at the same time it allows helpful, symbiotic bacteria, such as E. coli, to become established within the human body. From the time of the initial invasion of a foreign element until its removal, the entire immune systemincluding diverse types of white blood cells, each with a different responsibilityharmoniously functions together in recognizing, attacking, and destroying substances identified as foreign.

The immune system is often divided into two sections:

Another way of categorizing this is "nonspecific defenses" (skin, mucous membranes, phagocytes, fever, interferons, cilia, and stomach acid) and "specific defenses" (the cell-mediated and the humoral systems, both of which attack specific pathogens).

The adaptive immune system, also called the "acquired immune system, and "specific immune system," ensures that animals that survive an initial infection by a pathogen are generally immune to further illness caused by that same pathogen. The adaptive immune system is based on dedicated immune cells termed leukocytes (white blood cells).

The basis of specific immunity lies in the capacity of immune cells to distinguish between proteins produced by the body's own cells ("self" antigenthose of the original organism), and proteins produced by invaders or cells under control of a virus ("non-self" antigenor, what is not recognized as the original organism). This distinction is made via T-Cell Receptors (TCR) or B-Cell Receptors (BCR). For these receptors to be efficient they must be produced in thousands of configurations; this way they are able to distinguish between many different invader proteins.

This immense diversity of receptors would not fit in the genome of a cell, and millions of genes, one for each type of possible receptor, would be impractical. Instead, there are a few families of genes, each one having a slightly different modification. Through a special process, unique to cells of jawed vertebrates (Gnathostomata), the genes in these T-cell and B-cell lymphocytes recombine, one from each family, arbitrarily into a single gene.

This way, for example, each antibody or BCR of B lymphocytes has six portions, and is created from two genes unique to this lymphocyte, created by the recombination (union) of a random gene from each family. If there are 6 families, with 50, 30, 9, 40, and 5 members, the total possible number of antibodies is 50x30x6x9x40x5 = 16 million. On top of this there are other complex processes that increase the diversity of BCR or TCR even more, by mutation of the genes in question. The variability of antibodies is practically limitless, and the immune system creates antibodies for any molecule, even artificial molecules that do not exist in nature.

Many TCR and BCR created this way will react with their own peptides. One of the functions of the thymus and bone marrow is to hold young lymphocytes until it is possible to determine which ones react to molecules of the organism itself. This is done by specialized cells in these organs that present the young lymphocytes with molecules produced by them (and effectively the body). All the lymphocytes that react to them are destroyed, and only those that show themselves to be indifferent to the body are released into the bloodstream.

The lymphocytes that do not react to the body number in the millions, each with millions of possible configurations of receptors, each with a receptor for different parts of each microbial protein possible. The vast majority of lymphocytes never find a protein that its receptor is specified for, those few that do find one are stimulated to reproduce. Effective cells are generated with the specific receptor and memory cells. These memory cells are quiescent, they have long lives and are capable of identifying this antigen some time later, multiplying themselves quickly and rapidly responding to future infections.

In many species, the adaptive immune system can be divided into two major sections, the humoral immune system and the cell-mediated immune system.

The humoral immune system acts against bacteria and viruses in the body liquids (e.g., blood) by means of proteins, called immunoglobulins (also known as antibodies), which are produced by B cells. B cells are lymphocytes, with the "B" standing for the bursa of Fabricius, an organ unique to birds, where avian B cells mature. (It does not stand for bone marrow, where B cells are produced in all other vertebrates except for rabbits. B cells were original observed in studies done on immunity in chickens.)

Secreted antibodies bind to antigens on the surfaces of invading microbes (such as viruses or bacteria), which flags them for destruction. An antigen is any substance that causes the immune system to produce antibodies.

Humoral immunity refers to antibody production and all the accessory processes that accompany it: Th2 (T-helper 2 cells) activation and cytokine production (cytokines are proteins that affect the interaction between cells); germinal center formation and isotype switching (switching a specific region of the antibody); and affinity maturation and memory cell generation (memory cell generation has to do with the ability for a body to "remember" a pathogen by producing antibodies specifically targeted for it). Humoral immunity also refers to the effector functions of antibodies, which include pathogen and toxin neutralization, classical complement activation, and opsonin promotion of phagocytosis and pathogen elimination.

The human body has the ability to form millions of different types of B cells each day, and each type has a unique receptor protein, referred to as the B cell receptor (BCR), on its membrane that will bind to one particular antigen. At any one time in the human body there are B cells circulating in the blood and lymph, but are not producing antibodies. Once a B cell encounters its cognate antigen and receives an additional signal from a helper T cell, it can further differentiate into one of two types of B cells.

B cells need two signals to initiate activation. Most antigens are T-dependent, meaning T cell help is required for maximum antibody production. With a T-dependent antigen, the first signal comes from antigen cross linking BCR (B cell receptor) and the second from the Th2 cell. T-dependent antigens present peptides on B cell Class II MHC proteins to Th2 cells. This triggers B cell proliferation and differentiation into plasma cells. Isotype switching to IgG, IgA, and IgE and memory cell generation occur in response to T-dependent antigens.

Some antigens are T-independent, meaning they can deliver both the antigen and the second signal to the B cell. Mice without a thymus (nude or athymic mice) can respond to T-independent antigens. Many bacteria have repeating carbohydrate epitopes that stimulate B cells to respond with IgM synthesis in the absence of T cell help.

T-dependent responses require that B cells and their Th2 cells respond to epitopes on the same antigen. T and B cell epitopes are not necessarily identical. (Once virus-infected cells have been killed and unassembled virus proteins released, B cells specific for internal proteins can also be activated to make opsonizing antibodies to those proteins.) Attaching a carbohydrate to a protein can convert the carbohydrate into a T-dependent antigen; the carbohydrate-specific B cell internalizes the complex and presents peptides to Th2 cells, which in turn activate the B cell to make antibodies specific for the carbohydrate.

An antibody is a large Y-shaped protein used to identify and neutralize foreign objects like bacteria and viruses. Production of antibodies and associated processes constitutes the humoral immune system. Each antibody recognizes a specific antigen unique to its target. This is because at the two tips of its "Y," it has structures akin to locks. Every lock only has one key, in this case, its own antigen. When the key is inserted into the lock, the antibody activates, tagging or neutralizing its target. The production of antibodies is the main function of the humoral immune system.

Immunoglobulins are glycoproteins in the immunoglobulin superfamily that function as antibodies. The terms antibody and immunoglobulin are often used interchangeably. They are found in the blood and tissue fluids, as well as many secretions. In structure, they are globulins (in the -region of protein electrophoresis). They are synthesized and secreted by plasma cells that are derived from the B cells of the immune system. B cells are activated upon binding to their specific antigen and differentiate into plasma cells. In some cases, the interaction of the B cell with a T helper cell is also necessary.

In humans, there are five types: IgA, IgD, IgE, IgG, and IgM. (Ig stands for immunoglobulin.). This is according to differences in their heavy chain constant domains. (The isotypes are also defined with light chains, but they do not define classes, so they are often neglected.) Other immune cells partner with antibodies to eliminate pathogens depending on which IgG, IgA, IgM, IgD, and IgE constant binding domain receptors it can express on its surface.

The antibodies that a single B lymphocyte produces can differ in their heavy chain, and the B cell often expresses different classes of antibodies at the same time. However, they are identical in their specificity for antigen, conferred by their variable region. To achieve the large number of specificities the body needs to protect itself against many different foreign antigens, it must produce millions of B lymphoyctes. In order to produce such a diversity of antigen binding sites for each possible antigen, the immune system would require many more genes than exist in the genome. It was Susumu Tonegawa who showed in 1976 that portions of the genome in B lymphocytes can recombine to form all the variation seen in the antibodies and more. Tonegawa won the Nobel Prize in Physiology or Medicine in 1987 for his discovery.

The cell-mediated immune system, the second main mechanism of the adaptive immune system, destroys virus-infected cells (among other duties) with T cells, also called "T lymphocytes." ("T" stands for thymus, where their final stage of development occurs.)

Cell-mediated immunity is an immune response that does not involve antibodies but rather involves the activation of macrophages and natural killer cells, the production of antigen-specific cytotoxic T-lymphocytes, and the release of various cytokines in response to an antigen. Cellular immunity protects the body by:

Cell-mediated immunity is directed primarily at microbes that survive in phagocytes and microbes that infect non-phagocytic cells. It is most effective in removing virus-infected cells, but also participates in defending against fungi, protozoans, cancers, and intracellular bacteria. It also plays a major role in transplant rejection.

There are two major types of T cells:

In addition, there are regulatory T cells (Treg cells) which are important in regulating cell-mediated immunity.

The adaptive immune system could take days or weeks after an initial infection to have an effect. However, most organisms are under constant assault from pathogens that must be kept in check by the faster-acting innate immune system. Innate immunity, or non-specific defense, defends against pathogens by rapid responses coordinated through chemical or physical barriers or "innate" receptors that recognize a wide spectrum of conserved pathogenic components.

In evolutionary time, it appears that the adaptive immune system developed abruptly in jawed fish. Prior to jawed fish, there is no evidence of adaptive immunity, and animals therefore relied only on their innate immunity. Plants, on the other hand, rely on secondary metabolites (chemical compounds in organisms that are not directly involved in the normal growth, development, or reproduction of organisms) to defend themselves against fungal and viral pathogens as well as insect herbivory. Plant secondary metabolites are derived through vast arrays of plant biosynthetic pathways not needed directly for plant survival, hence why they are named secondary. Plant secondary metabolism should not be confused with innate or adaptive immunity as they evolved along an entirely different evolutionary lineages and rely on entirely different signal cues, pathways, and responses.

The innate immune system, when activated, has a wide array of effector cells and mechanisms. There are several different types of phagocytic cells, which ingest and destroy invading pathogens. The most common phagocytes are neutrophils, macrophages, and dendritic cells. Another cell type, natural killer cells, are especially adept at destroying cells infected with viruses. Another component of the innate immune system is known as the complement system. Complement proteins are normally inactive components of the blood. However, when activated by the recognition of a pathogen or antibody, the various proteins recruit inflammatory cells, coat pathogens to make them more easily phagocytosed, and make destructive pores in the surfaces of pathogens.

The first-line defense includes barriers to infection, such as skin, the mucous coating of the gut, and airways. These physically prevent the interaction between the host and the pathogen. Pathogens that penetrate these barriers encounter constitutively expressed (constantly expressed) anti-microbial molecules (e.g., lysozymes) that restrict the infection.

In addition to the usual defense, the stomach secretes gastric acid, which, in addition to aiding digestive enzymes in the stomach to work on food, prevents bacterial colonization by most pathogens.

The second-line defense includes phagocytic cells (macrophages and neutrophil granulocytes) that can engulf (phagocytose) foreign substances. Macrophages are thought to mature continuously from circulating monocytes.

Phagocytosis involves chemotaxis, where phagocytic cells are attracted to microorganisms by means of chemotactic chemicals such as microbial products, complement, damaged cells, and white blood cell fragments. Chemotaxis is followed by adhesion, where the phagocyte sticks to the microorganism. Adhesion is enhanced by opsonization, where proteins like opsonins are coated on the surface of the bacterium. This is followed by ingestion, in which the phagocyte extends projections, forming pseudopods that engulf the foreign organism. Finally, the bacterium is digested by the enzymes in the lysosome, exposing it to reactive oxygen species and proteases.

In addition, anti-microbial proteins may be activated if a pathogen passes through the barrier offered by skin. There are several classes of antimicrobial proteins, such as acute phase proteins (C-reactive protein, for example, enhances phagocytosis and activates complement when it binds itself to the C-protein of S. pneumoniae ), lysozyme, and the complement system.

The complement system is a very complex group of serum proteins, which is activated in a cascade fashion. Three different pathways are involved in complement activation:

A cascade of protein activity follows complement activation; this cascade can result in a variety of effects, including opsonization of the pathogen, destruction of the pathogen by the formation and activation of the membrane attack complex, and inflammation.

Interferons are also anti-microbial proteins. These molecules are proteins that are secreted by virus-infected cells. These proteins then diffuse rapidly to neighboring cells, inducing the cells to inhibit the spread of the viral infection. Essentially, these anti-microbial proteins act to prevent the cell-to-cell proliferation of viruses.

Earlier studies of innate immunity utilized model organisms that lack adaptive immunity, such as the plant Arabidopsis thaliana, the fly Drosophila melanogaster, and the worm Caenorhabditis elegans. Advances have since been made in the field of innate immunology with the discovery of toll-like receptors (TLRs) and the intracellular nucleotide-binding site leucine-rich repeat proteins (NODs). NODs are receptors in mammal cells that are responsible for a large proportion of the innate immune recognition of pathogens.

In 1989, prior to the discovery of mammalian TLRs, Charles Janeway conceptualized and proposed that evolutionarily conserved features of infectious organisms were detected by the immune system through a set of specialized receptors, which he termed pathogen-associated molecular patterns (PAMPs) and pattern recognition receptors (PRRs), respectively. This insight was only fully appreciated after the discovery of TLRs by the Janeway lab in 1997. The TLRs now comprise the largest family of innate immune receptors (or PRRs). Janeways hypothesis has come to be known as the "stranger model" and substantial debate in the field persists to this day as to whether or not the concept of PAMPs and PRRs, as described by Janeway, is truly suitable to describe the mechanisms of innate immunity. The competing "danger model" was proposed in 1994 by Polly Matzinger and argues against the focus of the stranger model on microbial derived signals, suggesting instead that endogenous danger/alarm signals from distressed tissues serve as the principle purveyors of innate immune responses.

Both models are supported in the later literature, with discoveries that substances of both microbial and non-microbial sources are able to stimulate innate immune responses, which has led to increasing awareness that perhaps a blend of the two models would best serve to describe the currently known mechanisms governing innate immunity.

Splitting the immune system into innate and adaptive systems simplifies discussions of immunology. However, the systems actually are quite intertwined in a number of important respects.

One important example is the mechanisms of "antigen presentation." After they leave the thymus, T cells require activation to proliferate and differentiate into cytotoxic ("killer") T cells (CTLs). Activation is provided by antigen-presenting cells (APCs), a major category of which are the dendritic cells. These cells are part of the innate immune system.

Activation occurs when a dendritic cell simultaneously binds itself to a T "helper" cell's antigen receptor and to its CD28 receptor, which provides the "second signal" needed for DC activation. This signal is a means by which the dendritic cell conveys that the antigen is indeed dangerous, and that the next encountered T "killer" cells need to be activated. This mechanism is based on antigen-danger evaluation by the T cells that belong to the adaptive immune system. But the dendritic cells are often directly activated by engaging their toll-like receptors, getting their "second signal" directly from the antigen. In this way, they actually recognize in "first person" the danger, and direct the T killer attack. In this respect, the innate immune system therefore plays a critical role in the activation of the adaptive immune system.

Adjuvants, or chemicals that stimulate an immune response, provide artificially this "second signal" in procedures when an antigen that would not normally raise an immune response is artificially introduced into a host. With the adjuvant, the response is much more robust. Historically, a commonly-used formula is Freund's Complete Adjuvant, an emulsion of oil and mycobacterium. It was later discovered that toll-like receptors, expressed on innate immune cells, are critical in the activation of adaptive immunity.

Many factors can contribute to the general weakening of the immune system:

Despite high hopes, there are no medications that directly increase the activity of the immune system. Various forms of medication that activate the immune system may cause autoimmune disorders.

Suppression of the immune system is often used to control autoimmune disorders or inflammation when this causes excessive tissue damage, and to prevent transplant rejection after an organ transplant. Commonly used immunosuppressants include glucocorticoids, azathioprine, methotrexate, ciclosporin, cyclophosphamide, and mercaptopurine. In organ transplants, ciclosporin, tacrolimus, mycophenolate mofetil, and various others are used to prevent organ rejection through selective T cell inhibition.

The most important function of the human immune system occurs at the cellular level of the blood and tissues. The lymphatic and blood circulation systems are highways for specialized white blood cells to travel around the body. Each white blood cell type (B cells, T cells, natural killer cells, and macrophages) has a different responsibility, but all function together with the primary objective of recognizing, attacking, and destroying bacteria, viruses, cancer cells, and all substances seen as foreign. Without this coordinated effort, a person would not be able to survive more than a few days before succumbing to overwhelming infection.

Infections set off an alarm that alerts the immune system to bring out its defensive weapons. Natural killer cells and macrophages rush to the scene to consume and digest infected cells. If the first line of defense fails to control the threat, antibodies, produced by the B cells, upon the order of T helper cells, are custom-designed to hone in on the invader.

Many disorders of the human immune system fall into two broad categories that are characterized by:

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Immune system - New World Encyclopedia

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Innate immune system – Wikipedia, the free encyclopedia

Monday, August 31st, 2015

The innate immune system, also known as the nonspecific immune system,[1] is an important subsystem of the overall immune system that comprises the cells and mechanisms that defend the host from infection by other organisms. The cells of the innate system recognize and respond to pathogens in a generic way, but, unlike the adaptive immune system (which is found only in vertebrates), it does not confer long-lasting or protective immunity to the host.[2] Innate immune systems provide immediate defense against infection, and are found in all classes of plant and animal life. They include both humoral immunity components and cell-mediated immunity components.

The innate immune system is an evolutionarily older defense strategy, and is the dominant immune system found in plants, fungi, insects, and primitive multicellular organisms.[3]

The major functions of the vertebrate innate immune system include:

Anatomical barriers include physical, chemical and biological barriers. The epithelial surfaces form a physical barrier that is impermeable to most infectious agents, acting as the first line of defense against invading organisms.[4]Desquamation of skin epithelium also helps remove bacteria and other infectious agents that have adhered to the epithelial surfaces. Lack of blood vessels and inability of the epidermis to retain moisture, presence of sebaceous glands in the dermis provides an environment unsuitable for the survival of microbes.[4] In the gastrointestinal and respiratory tract, movement due to peristalsis or cilia, respectively, helps remove infectious agents.[4] Also, mucus traps infectious agents.[4] The gut flora can prevent the colonization of pathogenic bacteria by secreting toxic substances or by competing with pathogenic bacteria for nutrients or attachment to cell surfaces.[4] The flushing action of tears and saliva helps prevent infection of the eyes and mouth.[4]

Inflammation is one of the first responses of the immune system to infection or irritation. Inflammation is stimulated by chemical factors released by injured cells and serves to establish a physical barrier against the spread of infection, and to promote healing of any damaged tissue following the clearance of pathogens.[5]

The process of acute inflammation is initiated by cells already present in all tissues, mainly resident macrophages, dendritic cells, histiocytes, Kupffer cells, and mastocytes. These cells present receptors, contained on the surface or within the cell, named pattern recognition receptors (PRRs), which recognise molecules that are broadly shared by pathogens but distinguishable from host molecules, collectively referred to as pathogen-associated molecular patterns (PAMPs). At the onset of an infection, burn, or other injuries, these cells undergo activation (one of their PRRs recognizes a PAMP) and release inflammatory mediators responsible for the clinical signs of inflammation.

Chemical factors produced during inflammation (histamine, bradykinin, serotonin, leukotrienes, and prostaglandins) sensitize pain receptors, cause vasodilation of the blood vessels at the scene, and attract phagocytes, especially neutrophils.[5] Neutrophils then trigger other parts of the immune system by releasing factors that summon other leukocytes and lymphocytes. Cytokines produced by macrophages and other cells of the innate immune system mediate the inflammatory response. These cytokines include TNF, HMGB1, and IL-1.[6]

The inflammatory response is characterized by the following symptoms:

The complement system is a biochemical cascade of the immune system that helps, or complements, the ability of antibodies to clear pathogens or mark them for destruction by other cells. The cascade is composed of many plasma proteins, synthesised in the liver, primarily by hepatocytes. The proteins work together to:

Elements of the complement cascade can be found in many nonmammalian species including plants, birds, fish, and some species of invertebrates.[7]

All white blood cells (WBC) are known as leukocytes. Leukocytes are different from other cells of the body in that they are not tightly associated with a particular organ or tissue; thus, they function similar to independent, single-cell organisms. Leukocytes are able to move freely and interact with and capture cellular debris, foreign particles, or invading microorganisms. Unlike many other cells in the body, most innate immune leukocytes cannot divide or reproduce on their own, but are the products of multipotent hematopoietic stem cells present in the bone marrow.[2]

The innate leukocytes include: Natural killer cells, mast cells, eosinophils, basophils; and the phagocytic cells including macrophages, neutrophils, and dendritic cells, and function within the immune system by identifying and eliminating pathogens that might cause infection.[3]

Mast cells are a type of innate immune cell that reside in connective tissue and in the mucous membranes. They are intimately associated with wound healing and defense against pathogens, but are also often associated with allergy and anaphylaxis.[5] When activated, mast cells rapidly release characteristic granules, rich in histamine and heparin, along with various hormonal mediators, and chemokines, or chemotactic cytokines into the environment. Histamine dilates blood vessels, causing the characteristic signs of inflammation, and recruits neutrophils and macrophages.[5]

The word 'phagocyte' literally means 'eating cell'. These are immune cells that engulf, i.e. phagocytose, pathogens or particles. To engulf a particle or pathogen, a phagocyte extends portions of its plasma membrane, wrapping the membrane around the particle until it is enveloped (i.e., the particle is now inside the cell). Once inside the cell, the invading pathogen is contained inside an endosome, which merges with a lysosome.[3] The lysosome contains enzymes and acids that kill and digest the particle or organism. In general, phagocytes patrol the body searching for pathogens, but are also able to react to a group of highly specialized molecular signals produced by other cells, called cytokines. The phagocytic cells of the immune system include macrophages, neutrophils, and dendritic cells.

Phagocytosis of the hosts own cells is common as part of regular tissue development and maintenance. When host cells die, either internally induced by processes involving programmed cell death (also called apoptosis) or caused by cell injury due to a bacterial or viral infection, phagocytic cells are responsible for their removal from the affected site.[2] By helping to remove dead cells preceding growth and development of new healthy cells, phagocytosis is an important part of the healing process following tissue injury.

Macrophages, from the Greek, meaning "large eaters," are large phagocytic leukocytes, which are able to move outside of the vascular system by moving across the walls of capillary vessels and entering the areas between cells in pursuit of invading pathogens. In tissues, organ-specific macrophages are differentiated from phagocytic cells present in the blood called monocytes. Macrophages are the most efficient phagocytes, and can phagocytose substantial numbers of bacteria or other cells or microbes.[3] The binding of bacterial molecules to receptors on the surface of a macrophage triggers it to engulf and destroy the bacteria through the generation of a respiratory burst, causing the release of reactive oxygen species. Pathogens also stimulate the macrophage to produce chemokines, which summons other cells to the site of infection.[3]

Neutrophils, along with two other cell types; eosinophils and basophils (see below), are known as granulocytes due to the presence of granules in their cytoplasm, or as polymorphonuclear cells (PMNs) due to their distinctive lobed nuclei. Neutrophil granules contain a variety of toxic substances that kill or inhibit growth of bacteria and fungi. Similar to macrophages, neutrophils attack pathogens by activating a respiratory burst. The main products of the neutrophil respiratory burst are strong oxidizing agents including hydrogen peroxide, free oxygen radicals and hypochlorite. Neutrophils are the most abundant type of phagocyte, normally representing 50 to 60% of the total circulating leukocytes, and are usually the first cells to arrive at the site of an infection.[5] The bone marrow of a normal healthy adult produces more than 100 billion neutrophils per day, and more than 10 times that many per day during acute inflammation.[5]

Dendritic cells (DC) are phagocytic cells present in tissues that are in contact with the external environment, mainly the skin (where they are often called Langerhans cells), and the inner mucosal lining of the nose, lungs, stomach, and intestines.[2] They are named for their resemblance to neuronal dendrites, but dendritic cells are not connected to the nervous system. Dendritic cells are very important in the process of antigen presentation, and serve as a link between the innate and adaptive immune systems.

Basophils and eosinophils are cells related to the neutrophil (see above). When activated by a pathogen encounter, basophils releasing histamine are important in defense against parasites, and play a role in allergic reactions (such as asthma).[3] Upon activation, eosinophils secrete a range of highly toxic proteins and free radicals that are highly effective in killing bacteria and parasites, but are also responsible for tissue damage occurring during allergic reactions. Activation and toxin release by eosinophils is, therefore, tightly regulated to prevent any inappropriate tissue destruction.[5]

Natural killer cells, or NK cells, are a component of the innate immune system that does not directly attack invading microbes. Rather, NK cells destroy compromised host cells, such as tumor cells or virus-infected cells, recognizing such cells by a condition known as "missing self." This term describes cells with abnormally low levels of a cell-surface marker called MHC I (major histocompatibility complex) - a situation that can arise in viral infections of host cells.[7] They were named "natural killer" because of the initial notion that they do not require activation in order to kill cells that are "missing self." For many years, it was unclear how NK cell recognize tumor cells and infected cells. It is now known that the MHC makeup on the surface of those cells is altered and the NK cells become activated through recognition of "missing self". Normal body cells are not recognized and attacked by NK cells because they express intact self MHC antigens. Those MHC antigens are recognized by killer cell immunoglobulin receptors (KIR) that, in essence, put the brakes on NK cells. The NK-92 cell line does not express KIR and is developed for tumor therapy.[8][9][10][11]

Like other 'unconventional' T cell subsets bearing invariant T cell receptors (TCRs), such as CD1d-restricted Natural Killer T cells, T cells exhibit characteristics that place them at the border between innate and adaptive immunity. On one hand, T cells may be considered a component of adaptive immunity in that they rearrange TCR genes to produce junctional diversity and develop a memory phenotype. However, the various subsets may also be considered part of the innate immune system where a restricted TCR or NK receptors may be used as a pattern recognition receptor. For example, according to this paradigm, large numbers of V9/V2 T cells respond within hours to common molecules produced by microbes, and highly restricted intraepithelial V1 T cells will respond to stressed epithelial cells.

The coagulation system overlaps with the immune system. Some products of the coagulation system can contribute to the non-specific defenses by their ability to increase vascular permeability and act as chemotactic agents for phagocytic cells. In addition, some of the products of the coagulation system are directly antimicrobial. For example, beta-lysine, a protein produced by platelets during coagulation, can cause lysis of many Gram-positive bacteria by acting as a cationic detergent.[4] Many acute-phase proteins of inflammation are involved in the coagulation system.

Also increased levels of lactoferrin and transferrin inhibit bacterial growth by binding iron, an essential nutrient for bacteria.[4]

The innate immune response to infectious and sterile injury is modulated by neural circuits that control cytokine production period. The Inflammatory Reflex is a prototypical neural circuit that controls cytokine production in spleen.[12] Action potentials transmitted via the vagus nerve to spleen mediate the release of acetylcholine, the neurotransmitter that inhibits cytokine release by interacting with alpha7 nicotinic acetylcholine receptors (CHRNA7) expressed on cytokine-producing cells.[13] The motor arc of the inflammatory reflex is termed the cholinergic anti-inflammatory pathway.

The parts of the innate immune system have different specificity for different pathogens.

Cells of the innate immune system, in effect, prevent free growth of bacteria within the body; however, many pathogens have evolved mechanisms allowing them to evade the innate immune system.[15][16]

Evasion strategies that circumvent the innate immune system include intracellular replication, such as in Mycobacterium tuberculosis, or a protective capsule that prevents lysis by complement and by phagocytes, as in salmonella.[17]Bacteroides species are normally mutualistic bacteria, making up a substantial portion of the mammalian gastrointestinal flora.[18] Some species (B. fragilis, for example) are opportunistic pathogens, causing infections of the peritoneal cavity. These species evade the immune system through inhibition of phagocytosis by affecting the receptors that phagocytes use to engulf bacteria or by mimicking host cells so that the immune system does not recognize them as foreign. Staphylococcus aureus inhibits the ability of the phagocyte to respond to chemokine signals. Other organisms such as M. tuberculosis, Streptococcus pyogenes, and Bacillus anthracis utilize mechanisms that directly kill the phagocyte.

Bacteria and fungi may also form complex biofilms, providing protection from the cells and proteins of the immune system; recent studies indicate that such biofilms are present in many successful infections, including the chronic Pseudomonas aeruginosa and Burkholderia cenocepacia infections characteristic of cystic fibrosis.[19]

Type I interferons (IFN), secreted mainly by dendritic cells,[20] play the central role in antiviral host defense and creation of an effective antiviral state in a cell.[21] Viral components are recognized by different receptors: Toll-like receptors are located in the endosomal membrane and recognize double-stranded RNA (dsRNA), MDA5 and RIG-I receptors are located in the cytoplasm and recognize long dsRNA and phosphate-containing dsRNA respectively.[22] The viral recognition by MDA5 and RIG-I receptors in the cytoplasm induces a conformational change between the caspase-recruitment domain (CARD) and the CARD-containing adaptor MAVS. In parallel, the viral recognition by toll-like receptors in the endocytic compartments induces the activation of the adaptor protein TRIF. These two pathways converge in the recruitment and activation of the IKK/TBK-1 complex, inducing phosphorylation and homo- and hetero-dimerization of transcription factors IRF3 and IRF7. These molecules are translocated in the nucleus, where they induce IFN production with the presence of C-Jun (a particular transcription factor) and activating transcription factor 2. IFN then binds to the IFN receptors, inducing expression of hundreds of interferon-stimulated genes. This leads to production of proteins with antiviral properties, such as protein kinase R, which inhibits viral protein synthesis, or the 2,5-oligoadenylate synthetase family, which degrades viral RNA. These molecules establish an antiviral state in the cell.[21]

Some viruses are able to evade this immune system by producing molecules that interfere with the IFN production pathway. For example, the Influenza A virus produces NS1 protein, which can bring to single-stranded and double-stranded RNA, thus inhibiting type I IFN production. Influenza A virus also blocks protein kinase R activation and the establishment of the antiviral state.[23] The dengue virus also inhibits type I IFN production by blocking IRF-3 phosophorylation using NS2B3 protease complex.[24]

Bacteria (and perhaps other prokaryotic organisms), utilize a unique defense mechanism, called the restriction modification system to protect themselves from pathogens, such as bacteriophages. In this system, bacteria produce enzymes, called restriction endonucleases, that attack and destroy specific regions of the viral DNA of invading bacteriophages. Methylation of the host's own DNA marks it as "self" and prevents it from being attacked by endonucleases.[25] Restriction endonucleases and the restriction modification system exist exclusively in prokaryotes.

Invertebrates do not possess lymphocytes or an antibody-based humoral immune system, and it is likely that a multicomponent, adaptive immune system arose with the first vertebrates.[26] Nevertheless, invertebrates possess mechanisms that appear to be precursors of these aspects of vertebrate immunity. Pattern recognition receptors are proteins used by nearly all organisms to identify molecules associated with microbial pathogens. Toll-like receptors are a major class of pattern recognition receptor, that exists in all coelomates (animals with a body-cavity), including humans.[27] The complement system, as discussed above, is a biochemical cascade of the immune system that helps clear pathogens from an organism, and exists in most forms of life. Some invertebrates, including various insects, crabs, and worms utilize a modified form of the complement response known as the prophenoloxidase (proPO) system.[26]

Antimicrobial peptides are an evolutionarily conserved component of the innate immune response found among all classes of life and represent the main form of invertebrate systemic immunity. Several species of insect produce antimicrobial peptides known as defensins and cecropins.

In invertebrates, pattern recognition proteins (PRPs) trigger proteolytic cascades that degrade proteins and control many of the mechanisms of the innate immune system of invertebratesincluding hemolymph coagulation and melanization. Proteolytic cascades are important components of the invertebrate immune system because they are turned on more rapidly than other innate immune reactions because they do not rely on gene changes. Proteolytic cascades have been found to function the same in both vertebrate and invertebrates, even though different proteins are used throughout the cascades.[28]

In the hemolymph, which makes up the fluid in the circulatory system of arthropods, a gel-like fluid surrounds pathogen invaders, similar to the way blood does in other animals. There are various different proteins and mechanisms that are involved in invertebrate clotting. In crustaceans, transglutaminase from blood cells and mobile plasma proteins make up the clotting system, where the transglutaminase polymerizes 210 kDa subunits of a plasma-clotting protein. On the other hand, in the horseshoe crab species clotting system, components of proteolytic cascades are stored as inactive forms in granules of hemocytes, which are released when foreign molecules, like lipopolysaccharides enter.[28]

Members of every class of pathogen that infect humans also infect plants. Although the exact pathogenic species vary with the infected species, bacteria, fungi, viruses, nematodes, and insects can all cause plant disease. As with animals, plants attacked by insects or other pathogens use a set of complex metabolic responses that lead to the formation of defensive chemical compounds that fight infection or make the plant less attractive to insects and other herbivores.[29] (see: plant defense against herbivory).

Like invertebrates, plants neither generate antibody or T-cell responses nor possess mobile cells that detect and attack pathogens. In addition, in case of infection, parts of some plants are treated as disposable and replaceable, in ways that very few animals are able to do. Walling off or discarding a part of a plant helps stop spread of an infection.[29]

Most plant immune responses involve systemic chemical signals sent throughout a plant. Plants use pattern-recognition receptors to recognize conserved microbial signatures. This recognition triggers an immune response. The first plant receptors of conserved microbial signatures were identified in rice (XA21, 1995)[30][31] and in Arabidopsis (FLS2, 2000).[32] Plants also carry immune receptors that recognize highly variable pathogen effectors. These include the NBS-LRR class of proteins. When a part of a plant becomes infected with a microbial or viral pathogen, in case of an incompatible interaction triggered by specific elicitors, the plant produces a localized hypersensitive response (HR), in which cells at the site of infection undergo rapid programmed cell death to prevent the spread of the disease to other parts of the plant. HR has some similarities to animal pyroptosis, such as a requirement of caspase-1-like proteolytic activity of VPE, a cysteine protease that regulates cell disassembly during cell death.[33]

"Resistance" (R) proteins, encoded by R genes, are widely present in plants and detect pathogens. These proteins contain domains similar to the NOD Like Receptors and Toll-like receptors utilized in animal innate immunity. Systemic acquired resistance (SAR) is a type of defensive response that renders the entire plant resistant to a broad spectrum of infectious agents.[34] SAR involves the production of chemical messengers, such as salicylic acid or jasmonic acid. Some of these travel through the plant and signal other cells to produce defensive compounds to protect uninfected parts, e.g., leaves.[35] Salicylic acid itself, although indispensable for expression of SAR, is not the translocated signal responsible for the systemic response. Recent evidence indicates a role for jasmonates in transmission of the signal to distal portions of the plant. RNA silencing mechanisms are also important in the plant systemic response, as they can block virus replication.[36] The jasmonic acid response, is stimulated in leaves damaged by insects, and involves the production of methyl jasmonate.[29]

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The immune system and cancer | Cancer Research UK

Wednesday, August 19th, 2015

This page is about the immune system. It also tells you about the effects that cancer or treatments may have on the immune system. Some treatments can boost theimmune system tohelp fight cancer.There is information about

The immune system protects the body against illness and infection caused by bacteria, viruses, fungi or parasites. It is really a collection of reactions and responses that the body makes to damaged cells orinfection. So it is sometimes called the immune response.

The immune system is important to cancer patients in many ways because

Cancer can weaken the immune system by spreading into the bone marrow. The bone marrowmakesblood cells that help to fight infection. Weakening of the immune system happens most often in leukaemia or lymphoma. But it can happen with other cancers too. The cancer in the bone marrow stops the bone marrow making so many blood cells.

Chemotherapy, biological therapies andradiotherapy can temporarilyweaken immunity by causing a drop in the number of white blood cells made in the bone marrow. High doses of steroids can also weaken your immune system while you are taking them.

You can find information about the different types of cancer treatments.

Some cells of the immune system can recognise cancer cells as abnormal and kill them. Unfortunately, this may not beenough to get rid of a cancer altogether. But some new treatments aim to use the immune system to fight cancer.

There are two main parts of the immune system

This is also called innate immunity. These immune mechanisms are always ready and prepared to defend the body from infection. They can act immediately (or very quickly). This inbuilt protection comes from

There are several ways that these natural protection mechanisms can be damaged or overcome if you have cancer. For example

These white blood cells are very important for fighting infection.They can

Your normal neutrophil count is between 2,000 and 7,500 per cubic millimetre of blood. When you don't have enough neutrophils you are said to be neutropaenic.

Chemotherapy and some radiotherapy treatments can lower theneutrophil count. So, after chemotherapy, biological therapy and some types ofradiotherapy you may be more likely to get bacterial or fungal infections.

If you are having cancer treatment, it is important for you to know that

You are morelikely to become ill from bugs you carry around with you normally, not from catching someone else's. This means that you usually don't have to avoid your family, friends or children when you gohome after chemotherapy.

You can ask your cancer doctor or nurse what precautions you should take against infection.

When your blood counts are low, you may needto take antibiotics to help prevent severe infection.

This is immune protection thatthe body learns from being exposed to diseases. The body learns to recognise each different kind of bacteria, fungus orvirus it meets for the first time. The next time that particular bug tries to invade the body, the immune system is ready for it and able to fight it off more easily. This is why you usually only get some infectious diseases oncefor example, measles or chicken pox.

Vaccination works by using this type of immunity. A vaccine contains a small amount of protein from a disease. This is not harmful, but it allows the immune system to recognise the disease if it meets it again. The immune response can then stop you getting the disease. Some vaccines use tiny amounts of the live bacteria or virus. These are called live attenuated vaccines.

Attenuated means that the virus or bacteria has been changed so that it will stimulate the immune system to make antibodies but won't cause the infection. Other types of vaccine use killed bacteria or viruses, or parts of proteinsproduced by bacteria and viruses.

The white blood cells involved in the acquired immune response are called lymphocytes. There are two main types of lymphocytesB cells and T cells. B and T lymphocytes are made in the bone marrow, like the other blood cells.

Lymphocyteshave to fully mature before they can help in the immune response. B cells mature in the bone marrow. But the immature T cells travel through the bloodstream to the thymus gland where they become fully developed.

Once they are fully mature, the B and T cells travel to the spleen and lymph nodes ready to fight infection.

You can read about the thymus, spleen and lymph nodes on ourpage aboutthe lymphatic system and cancer.

B cells react against invading bacteria or viruses by making proteins called antibodies. The antibody made is different for each different type of germ (bug). The antibody locks onto the surface of the invading bacteria or virus. The invader is then marked with the antibody so that the body knows it is dangerous and it can be killed off. Antibodies can also detect and kill damaged cells.

The B cells are part of the memory of the immune system. The next time the same germtries to invade, the B cells that make the right antibody are ready for it. They are able to make their antibody very quickly.

Antibodies have two ends. One end sticks to proteins on the outside of white blood cells. The other end sticks to the germ or damaged cell and helps to kill it. The end of the antibody that sticks to the white blood cell is always the same. So it is called the constant end.

The end of the antibody that recognises germs and damaged cells varies depending on the cell it is designed to recognise. So it is called the variable end. Each B cell makes antibodies with a different variable end from other B cells.

Cancer cells are not normal cells. So some antibodies with variable ends recognise cancer cells and stick to them.

There are different kinds of T cells called

The helper T cells stimulate the B cells to make antibodies, and help killer cells develop.

Killer T cells kill the body's own cells that have been invaded by the viruses or bacteria. This prevents the germfrom reproducing in the cell and then infecting other cells.

Some cancertreatments use elements of the immune system to help treat cancer.

Immunotherapy is a type of biological therapy. Biological therapies use natural body substances or drugs made from natural body substances to treat cancer. Immunotherapies are treatments that use your immune system. They are helpful in cancer treatment because cancer cells are different from normal cells and so can be picked up by the immune system.

Many different chemicals produced as part of the immune response can now be made in the laboratory. These include interferon, interleukin 2 and monoclonal antibodies.

Interferon alpha and interleukin 2 act by boosting the immune response to help the body kill off cancer cells.

Scientists are also trying to develop vaccinations against cancer cells. It may be possible for the vaccine to train the immune system to see cancer cells as being invaders and kill them.

You can read more aboutbiological therapies.

Monoclonal antibodies are made in the laboratory. The scientists developing them make an antibody with a variable end that recognises cancer cells. Monoclonal means that all the antibodies are exactly the same type, with the same variable end.

The monoclonal antibodies recognise molecules on the outside of cancer cells. Different antibodies have to be made for different types of cancer, for example

The constant end of cancer treating monoclonal antibodies kills the cancer cells by marking them so that other immune system cells pick them out. The job of these other cells is to find antibody labelled cells and kill them.

Scientists can sometimes make the monoclonal antibody even better at killing cancer cells. They may attach a radioactive atom that delivers radiation directly to the cancer cells. Or they can attach a chemotherapy drug that is taken straight to the cancer cells by the monoclonal antibody.

Monoclonal antibodies are used for many types of cancer. You can find out moreabout monoclonal antibodies.

There is a lot of research going on into using immune system therapies to treat cancer. You can find information about monoclonal antibody trials on ourclinical trials database.

Many people with cancer believe that they should strengthen their immune systems to help beat the disease. There is a commonly held belief that reducing stress can help to strengthen our immune systems. This is the thinking behind some complementary therapies, such asusing relaxation techniques.

There is some scientific evidence that stress weakens our immunity. Two studies looking at whether stress affected cancer recurrence had conflicting results. While no one knows whether strengthening immunity can help to cure cancer, most doctors and nurses agree that reducing stress is a good thing to do.

While many life stresses cannot be avoided altogether, there are ways you can try to help yourself. Many complementary therapies such as meditation, massage and reflexology, can be very relaxing.

You can avoid getting run down and look after yourself by

You can find outaboutcomplementary therapies.

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The immune system and cancer | Cancer Research UK

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How Sleeping Can Affect Your Immune System

Wednesday, August 5th, 2015

By Dr. Mercola

Researchers have learned that circadian rhythmsthe 24-hour cycles known as your internal body clockare involved in everything from sleep to weight gain, mood disorders, and a variety of diseases.

Your body actually has many internal clocksin your brain, lungs, liver, heart and even your skeletal musclesand they all work to keep your body running smoothly by controlling temperature and the release of hormones.

It's well known that lack of sleep can increase your chances of getting sick. A new study shows just how direct that connection is.

The research found that the circadian clocks of mice control an essential immune system gene that helps their bodies sense and ward off bacteria and viruses. When levels of that particular gene, called toll-like receptor 9 (TLR9), were at their highest, the mice were better able to withstand infections.

Interestingly, when the researchers induced sepsis, the severity of the disease was dependent on the timing of the induction. Severity directly correlated with cyclical changes in TLR9.

According to the authors, this may help explain why septic patients are known to be at higher risk of dying between the hours of 2 am and 6 am.

Furthermore, they also discovered that when mice were vaccinated when TLR9 was peaking, they had an enhanced immune response to the vaccine. The researchers believe vaccine effectiveness could be altered depending on the time of day the vaccination is administered...

According to study author Erol Fikrig, professor of epidemiology at the Yale School of Medicinei:

"These findings not only unveil a novel, direct molecular link between circadian rhythms and the immune system, but also open a new paradigm in the biology of the overall immune response with important implications for the prevention and treatment of disease. Furthermore, patients in the ICU often have disturbed sleep patterns, due to noise, nocturnal light exposure and medications; it will be important to investigate how these factors influence TLR9 expression levels and immune responses."

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How Sleeping Can Affect Your Immune System

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Immune System News — ScienceDaily

Friday, July 24th, 2015

Alefacept Preserves Beta Cell Function in Some New-Onset Type 1 Diabetes Patients out to Two Years July 20, 2015 Individuals with new-onset type 1 diabetes who took two courses of alefacept (Amevive, Astellas Pharma Inc.) soon after diagnosis show preserved beta cell function after two years compared to those ... read more Antibiotic Exposure Could Increase the Risk of Juvenile Arthritis July 20, 2015 Taking antibiotics may increase the risk that a child will develop juvenile arthritis, according to a study. Researchers found that children who were prescribed antibiotics had twice the risk of ... read more Cholesterol Metabolism in Immune Cells Linked to HIV Progression July 17, 2015 Lower levels of cholesterol in certain immune cells -- a result of enhanced cholesterol metabolism within those cells -- may help explain why some HIV-infected people are able to naturally control ... read more July 17, 2015 A study in mice may identify new ways to treat immune thrombocytopenia. Immune thrombocytopenia, or ITP, is an autoimmune disease whereby the immune system sends antibodies to attack and destroy the ... read more July 16, 2015 In response to an infection, the immune system refines its defensive proteins, called antibodies, to better target an invader. New research has revealed two mechanisms that favor the selection of B ... read more July 16, 2015 Iron regulatory proteins play an important role in the body's immune system. Proteins responsible for controlling levels of iron in the body also play an important role in combating infection, ... read more HIV Uses Immune System's Own Tools to Suppress It July 15, 2015 A research team has made a significant discovery on how HIV escapes the body's antiviral responses. The team uncovered how an HIV viral protein known as Vpu tricks the immune system by using its ... read more Host Genetics Played a Role in Vaccine Efficacy in the RV144 HIV Vaccine Trial July 15, 2015 Host genetics played a role in protection against HIV infection in the landmark RV144 vaccine trial conducted in Thailand, research ... read more July 15, 2015 Immunologists have identified a distinct set of long-lived antibody-producing cells in the human bone marrow that function as an immune ... read more Magnetic Nanoparticles Could Be Key to Effective Immunotherapy July 15, 2015 In recent years, researchers have hotly pursued immunotherapy, a promising form of treatment that relies on harnessing and training the body's own immune system to better fight cancer and ... read more Why Does PTSD Increase the Risk of Cardiovascular Disease? July 15, 2015 A new review article finds that post-traumatic stress disorder (PTSD) leads to overactive nerve activity, dysfunctional immune response and activation of the hormone system that controls blood ... read more Scientific Curiosity and Preparedness for Emerging Pathogen Outbreaks July 14, 2015 An essay reflects on a career path that started with the study of a somewhat obscure mouse virus mice and ended up at the frontline of the SARS and MERS coronavirus ... read more Anti-Stress Hormone May Provide Indication of Breast Cancer Risk July 14, 2015 A new study shows that women with low levels of an anti-stress hormone have an increased risk of getting breast cancer. The study is the first of its kind on humans and confirms previous similar ... read more Aerosolized Vaccine Protects Primates Against Ebola July 13, 2015 Scientists have developed an inhalable vaccine that protects primates against ... read more Cancer Discovery Links Experimental Vaccine and Biological Treatment July 13, 2015 A new study has linked two seemingly unrelated cancer treatments that are both now being tested in clinical trials. One treatment is a vaccine that targets a structure on the outside of cancer cells, ... read more Skin Cancer Marker Plays Critical Role in Tumor Growth July 13, 2015 The protein keratin 17 -- the presence of which is used in the lab to detect and stage various types of cancers -- is not just a biomarker for the disease, but may play a critical role in tumor ... read more July 13, 2015 Immune cells that creep across blood vessels trigger potentially fatal bleeding in platelet-deficient mice, according to a new report. If the same is true in humans, blocking the passage of these ... read more Scientists Find Molecular Switch That Creates Long-Term Immunity July 13, 2015 Researchers have identified a protein responsible for preserving the antibody-producing cells that lead to long-term immunity after infection or ... read more July 10, 2015 The microbiota is involved in many mechanisms, including digestion, vitamin synthesis and host defense. It is well established that a loss of bacterial symbionts promotes the development of ... read more Multiple Myeloma Hides in Bones Like a Wolf in Sheep's Clothing July 9, 2015 Multiple myeloma uses a trick akin to a wolf in sheeps clothing to grow in and spread to new bone sites. By overexpressing Runx2, a gene that normally is a master regulator of bone formation, the ... read more

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Easy Immune System Health home page

Monday, July 13th, 2015

Strong and vibrant Immune System Health is the key to overcoming chronic health problems. My name is Kerri Knox. I've been a Registered Nurse in intensive care units and emergency rooms for over a decade and now, as a Functional Medicine Practitioner, a specific type of natural health care practitioner that focuses on remedying chronic and traditionally 'incurable' health problems in my private practice every day, I've learned exactly what it takes for you to overcome your chronic health problems. You can see more about my Functional Medicine Practice here.

Having worked in Emergency Rooms and Intensive Care Units for over 10 years as a Registered Nurse, I was confused and frustrated at the inability of 'Western Medicine' to actually help people to get well. It was great for broken bones and appendicitis, but not so great for those with chronic 'incurable' diseases, and I saw the same people in the hospital and in clinics over and over again trying to simply maintain their poor health and poor quality of life. This frustration over our 'sick care system' inspired me to DO something about actually getting people WELL and improving their health- and I found that creating strong Immune System Health is the absolute key to getting well, overcoming illness and maintaining VIBRANT health!

In fact, 'Western Medicine', also called allopathic medicine or traditional medicine is so focused on managing disease that most people don't even REALIZE that they can overcome their health problems. But after working with thousands of people with health problems, in person and through my website and forums, I can assure you that you absolutely can overcome or at least SIGNIFICANTLY improve your 'incurable' chronic health issues- without drugs. Now that you know that you HAVE a choice, if you are willing to take the first steps to wellness, I'm committed to helping you feel better!

I'll share Scientifically Sound, Well Researched Secrets with you that few doctors know. Some of these secrets, like:

are secrets that have successfully helped tens of thousands of people to REALLY get well, improve their immune system health and Stay well.

To Your Good Health, Kerri Knox Registered Nurse and Functional Medicine Practitioner

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Immune System: MedlinePlus – National Library of Medicine

Sunday, July 5th, 2015

To use the sharing features on this page, please enable JavaScript. Acquired Immunodeficiency Syndrome see HIV/AIDS Acute Lymphoblastic Leukemia see Acute Lymphocytic Leukemia Acute Lymphocytic Leukemia Addison Disease Adenoidectomy see Tonsils and Adenoids Adenoids see Tonsils and Adenoids Adenovirus Infections see Viral Infections Adrenal Insufficiency see Addison Disease Adult Immunization see Immunization AIDS see HIV/AIDS AIDS and Infections see HIV/AIDS and Infections AIDS and Pregnancy see HIV/AIDS and Pregnancy AIDS in Women see HIV/AIDS in Women AIDS Medicines see HIV/AIDS Medicines AIDS--Living With AIDS see Living with HIV/AIDS ALL see Acute Lymphocytic Leukemia Allergic Rhinitis see Allergy; Hay Fever Allergy Allergy, Food see Food Allergy Allergy, Latex see Latex Allergy Anaphylaxis see Allergy Anatomy Animal Bites Ankylosing Spondylitis Antimicrobial Resistance see Infectious Diseases Aplastic Anemia Asthma Asthma in Children Autoimmune Diseases Autoinflammatory Disorders see Autoimmune Diseases Bone Marrow Diseases Bone Marrow Transplantation Bronchial Asthma see Asthma Bullous Pemphigoid see Pemphigus Cat Bites see Animal Bites Chikungunya see Viral Infections Childhood Asthma see Asthma in Children Childhood Immunization Childhood Leukemia Chronic Granulomatous Disease see Immune System and Disorders Chronic Lymphocytic Leukemia Churg-Strauss Syndrome see Eosinophilic Disorders CLL see Chronic Lymphocytic Leukemia Communicable Diseases see Infectious Diseases Coxsackievirus Infections see Viral Infections Cryptosporidiosis Diabetes Type 1 Dog Bites see Animal Bites Dry Eye see Sjogren's Syndrome EBV Infections see Infectious Mononucleosis Enterovirus see Viral Infections Eosinophilia see Eosinophilic Disorders Eosinophilic Disorders Epstein-Barr Virus Infections see Infectious Mononucleosis Fanconi Anemia see Aplastic Anemia Food Allergy Giant Cell Arteritis Glandular Fever see Infectious Mononucleosis Hand, Foot, and Mouth Disease see Viral Infections Hay Fever HIV/AIDS HIV/AIDS and Infections HIV/AIDS and Pregnancy HIV/AIDS in Women HIV/AIDS Medicines HIV/AIDS--Living With see Living with HIV/AIDS Hives Hodgkin Disease Human Immunodeficiency Virus see HIV/AIDS Hypereosinophilic Syndrome see Eosinophilic Disorders Hypersensitivity see Allergy Immune System and Disorders Immunization Immunization, Childhood see Childhood Immunization Infections, Viral see Viral Infections Infectious Diseases Infectious Mononucleosis Insulin-Dependent Diabetes Mellitus see Diabetes Type 1 JRA see Juvenile Rheumatoid Arthritis Juvenile Diabetes see Diabetes Type 1 Juvenile Rheumatoid Arthritis Kawasaki Disease Latex Allergy Leukemia, Acute Lymphoblastic see Acute Lymphocytic Leukemia Leukemia, Acute Lymphocytic see Acute Lymphocytic Leukemia Leukemia, Childhood see Childhood Leukemia Leukemia, Chronic Lymphocytic see Chronic Lymphocytic Leukemia Living with HIV/AIDS Lupus Lymph Nodes see Lymphatic Diseases Lymphatic Diseases Lymphatic Obstruction see Lymphedema Lymphedema Lymphoma MDS see Myelodysplastic Syndromes Milk Allergy see Food Allergy Mono see Infectious Mononucleosis Mononucleosis see Infectious Mononucleosis Morphea see Scleroderma Mucocutaneous Lymph Node Syndrome see Kawasaki Disease Multiple Myeloma Myelodysplastic Syndromes Myeloproliferative Disorders see Bone Marrow Diseases Non-Hodgkin Lymphoma see Lymphoma Nut Allergy see Food Allergy Opportunistic Infections in AIDS see HIV/AIDS and Infections Peanut Allergy see Food Allergy Pemphigoid see Pemphigus Pemphigus Plasma-cell Myeloma see Multiple Myeloma Plasmacytoma see Multiple Myeloma Pneumocystis Infections Pollen Allergy see Hay Fever Pregnancy and AIDS see HIV/AIDS and Pregnancy PrEP (Pre-Exposure Prophylaxis) see HIV/AIDS Medicines Rheumatoid Arthritis Rheumatoid Spondylitis see Ankylosing Spondylitis Roseola see Viral Infections SCID see Immune System and Disorders Scleroderma Seasonal Allergies see Hay Fever Severe Combined Immunodeficiency see Immune System and Disorders Sjogren's Syndrome SLE see Lupus Snake Bites see Animal Bites Spleen Diseases Splenic Diseaess see Spleen Diseases Splenomegaly see Spleen Diseases Spondylitis, Ankylosing see Ankylosing Spondylitis Still's Disease see Juvenile Rheumatoid Arthritis Swollen Glands see Lymphatic Diseases Systemic Lupus Erythematosus see Lupus Systemic Sclerosis see Scleroderma Temporal Arteritis see Giant Cell Arteritis Thymus Cancer Tonsillectomy see Tonsils and Adenoids Tonsillitis see Tonsils and Adenoids Tonsils and Adenoids Type I Diabetes see Diabetes Type 1 Urticaria see Hives Vaccination see Childhood Immunization; Immunization Viral Infections Waldenstrom's Macroglobulinemia see Lymphoma

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Immune System: MedlinePlus - National Library of Medicine

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Lack of Sleep and the Immune System – WebMD

Sunday, July 5th, 2015

Lack of sleep affects your immune system.

Mother knows best -- at least it appears that way when it comes to lack of sleep. It turns out that lack of sleep really may make us more prone to catching colds and the flu. And that includes the H1N1 virus.

It is an old wives tale that if you dont sleep well, you will get sick, and there is some experimental data that shows this is true, says Diwakar Balachandran, MD, director of the Sleep Center at the University of Texas M.D. Anderson Cancer Center in Houston.

When Nightmares Won't Go Away

Yael Levy recalls having chronic nightmares as far back as elementary school, when she was living in Israel. The grandchild of Holocaust survivors, she says her dreams were filled with images of suffering and death. In one recurrent nightmare, Levy was trapped in a concentration camp, facing death. In another, she was drowning in deep water. At their worst, the nightmares occurred on an almost weekly basis, leaving her jittery and desperately fatigued. "I would wake up so terrified that I was afraid...

Read the When Nightmares Won't Go Away article > >

Some 50 million to 70 million American adults suffer from sleep disorders or the inability to stay awake and alert, according to the CDC. Though its not always easy to do, getting adequate sleep can help keep our immune systems primed for attack.

Not getting enough sleep has been linked to a laundry list of mental and physical health problems, including those that stem from an impaired immune system. Our immune system is designed to protect us from colds, flu, and other ailments, but when it is not functioning properly, it fails to do its job. The consequences can include more sick days.

The relationship between lack of sleep and our immune systems is not quite as straightforward as mom made it out to be, however. The immune system is pretty complex. It is made up of several types of cells and proteins that are charged with keeping foreign invaders such as colds or flu at bay.

A lot of studies show our T-cells go down if we are sleep deprived, Balachandran says. And inflammatory cytokines go up. ... This could potentially lead to the greater risk of developing a cold or flu.

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How Sleeping Can Affect Your Immune System – Mercola.com

Friday, July 3rd, 2015

By Dr. Mercola

Researchers have learned that circadian rhythmsthe 24-hour cycles known as your internal body clockare involved in everything from sleep to weight gain, mood disorders, and a variety of diseases.

Your body actually has many internal clocksin your brain, lungs, liver, heart and even your skeletal musclesand they all work to keep your body running smoothly by controlling temperature and the release of hormones.

It's well known that lack of sleep can increase your chances of getting sick. A new study shows just how direct that connection is.

The research found that the circadian clocks of mice control an essential immune system gene that helps their bodies sense and ward off bacteria and viruses. When levels of that particular gene, called toll-like receptor 9 (TLR9), were at their highest, the mice were better able to withstand infections.

Interestingly, when the researchers induced sepsis, the severity of the disease was dependent on the timing of the induction. Severity directly correlated with cyclical changes in TLR9.

According to the authors, this may help explain why septic patients are known to be at higher risk of dying between the hours of 2 am and 6 am.

Furthermore, they also discovered that when mice were vaccinated when TLR9 was peaking, they had an enhanced immune response to the vaccine. The researchers believe vaccine effectiveness could be altered depending on the time of day the vaccination is administered...

According to study author Erol Fikrig, professor of epidemiology at the Yale School of Medicinei:

"These findings not only unveil a novel, direct molecular link between circadian rhythms and the immune system, but also open a new paradigm in the biology of the overall immune response with important implications for the prevention and treatment of disease. Furthermore, patients in the ICU often have disturbed sleep patterns, due to noise, nocturnal light exposure and medications; it will be important to investigate how these factors influence TLR9 expression levels and immune responses."

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14.00-Immune-Adult – Social Security Administration

Friday, July 3rd, 2015

14.00 Immune System Disorders

A. What disorders do we evaluate under the immune system disorders listings?

1. We evaluate immune system disorders that cause dysfunction in one or more components of your immune system.

a. The dysfunction may be due to problems in antibody production, impaired cell-mediated immunity, a combined type of antibody/cellular deficiency, impaired phagocytosis, or complement deficiency.

b. Immune system disorders may result in recurrent and unusual infections, or inflammation and dysfunction of the body's own tissues. Immune system disorders can cause a deficit in a single organ or body system that results in extreme (that is, very serious) loss of function. They can also cause lesser degrees of limitations in two or more organs or body systems, and when associated with symptoms or signs, such as severe fatigue, fever, malaise, diffuse musculoskeletal pain, or involuntary weight loss, can also result in extreme limitation.

c. We organize the discussions of immune system disorders in three categories: Autoimmune disorders; Immune deficiency disorders, excluding human immunodeficiency virus (HIV) infection; and HIV infection.

2. Autoimmune disorders (14.00D). Autoimmune disorders are caused by dysfunctional immune responses directed against the body's own tissues, resulting in chronic, multisystem impairments that differ in clinical manifestations, course, and outcome. They are sometimes referred to as rheumatic diseases, connective tissue disorders, or collagen vascular disorders. Some of the features of autoimmune disorders in adults differ from the features of the same disorders in children.

3. Immune deficiency disorders, excluding HIV infection (14.00E). Immune deficiency disorders are characterized by recurrent or unusual infections that respond poorly to treatment, and are often associated with complications affecting other parts of the body. Immune deficiency disorders are classified as either primary (congenital) or acquired. Individuals with immune deficiency disorders also have an increased risk of malignancies and of having autoimmune disorders.

4. Human immunodeficiency virus (HIV) infection (14.00F). HIV infection may be characterized by increased susceptibility to opportunistic infections, cancers, or other conditions, as described in 14.08.

B. What information do we need to show that you have an immune system disorder? Generally,

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14.00-Immune-Adult - Social Security Administration

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Immune System – Cancer Fighting Strategies

Saturday, June 27th, 2015

The Immune System and Cancer - An Antibody (The Immunoglobulin)

Here are a few facts about the immune system and cancer. For most of your life, your immune system successfully fought cancerous cells, killing them as they developed. That's its job. In fact, the only job Natural Killer cells have is to kill cancer cells and viruses. For cancer to develop, your immune system must either be worn out, ineffective, unable to kill cancer cells as fast as they normally develop, or you must be exposed to a mass of cancer causing toxins, radiation or some such thing, that increase the rate of development of cancer cells to an abnormally high level that your immune system can't handle.

Either way, it is vital to strengthen the immune system in your battle against cancer . Especially if you are getting medical treatments that wipe out your immune system.

Many natural supplements support the immune system. This is why so many of them are touted as being able to help you beat cancer. If someone has an immune system that is almost able to handle the cancer, even a poor immune system supplement can be enough to improve the immune system to the extent that it beats cancer.

Of course, for folks with more seriously compromised immune systems, this supplement or group of supplements would not work well because they are in worse shape. This is why it can get so confusing in deciding what to use. When a supplement or procedure has been used for years, especially if it is popular, you'll hear how it has beat cancer.

But what you don't know is if it worked 2% of the time or 15% of the time. Given the number of people who die from cancer, the success rate of most of these supplements is fairly low. In this report we try to find and recommend the supplements that work the best, so that you have the greatest likelihood of success. It is easy to squander money and more importantly time, on products that won't get the job done.

The other concern is to make sure you do enough to wipe out the cancer. Cancer is not something to pussyfoot around with. While it is always hopeful and great to read about how someone took just one supplement and beat their cancer, and while that could happen to you, your odds of success are much higher if you take many different supplements in order to hit the cancer as hard as you can.

In order to determine which cancer fighting supplements are the most effective ones, we energetically test them for what we call their healing power. We have found this to be the most effective way of determining which supplements are likely to be the best to use. Our experience is that this works much better than taking a guess at what is good, and what isn't as good as it sounds.

When we started doing this we were surprised at how poorly the well known supplements and procedures tested. Many had been around for years and were popular, used by many patients and naturopaths, etc. But they actually weren't highly effective. Though they are good enough to help some people, and thus over time, produced plenty of testimonials, as you see in this report, we've been able to find many stronger products. Most of them new and thus unknown.

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Immune System - Cancer Fighting Strategies

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The Immune System | Health | Patient.co.uk

Monday, June 8th, 2015

What is the immune system?

We are surrounded by millions of bacteria, viruses and other microbes (germs) that have the potential to enter our bodies and cause harm. The immune system is the body's defence against pathogens (disease-causing microbes). The immune system is made up of non-specialised defences such as skin and the acidic juice produced by your stomach. But it also has some highly specialised defences which give you immunity against (resistance to) particular pathogens. These defences are special white blood cells called lymphocytes. Other types of white blood cells play an important part in defending your body against infection.

The lymphatic system is also part of the immune system. The lymphatic system is made up of a network of vessels (tubes) which carry fluid called lymph. It contains specialised lymph tissue and all of the structures dedicated to the production of lymphocytes.

The immune system is generally divided into two parts. The first part is the defences you are born with. These form what are known as the innate system.

The second part of your immune system, known as immunity, develops as you grow. Your immunity gives you protection against specific pathogens. Not only can this system recognise particular pathogens, it also has a memory of this. This means that if you encounter a certain pathogen twice, your immune system recognises it the second time around. This usually means your body responds quicker to fight off the infection.

The innate system is found in many different places around the body. First line of defence is your skin. Skin forms a waterproof barrier that prevents pathogens from entering the body. Your body cavities, such as the nose and mouth, are lined with mucous membranes. Mucous membranes produce sticky mucus which can trap bacteria and other pathogens. Other fluids produced by the body help to protect your internal layers from invasion by pathogens. Gastric juice produced by the stomach has high acidity which helps to kill off many of the bacteria in food. Saliva washes pathogens off your teeth and helps to reduce the amount of bacteria and other pathogens in your mouth.

If bacteria or other pathogens manage to get through these initial defences, they encounter a second line of defence. Most of these defences are present in your blood, either as specialised white blood cells or as chemicals released by your cells and tissues.

The second part of your immune system, the part that gives you immunity, involves the activation of lymphocytes. This will be described later on. Lymphocytes are found in your blood and also in specialised lymph tissue such as lymph nodes, the spleen and the thymus.

The first line of defence is your body's skin and mucous membranes, as mentioned above.

If pathogens manage to get through these barriers, they encounter special white blood cells present in your bloodstream. There are different types of white cells, called neutrophils (polymorphs), lymphocytes, eosinophils, monocytes, and basophils.

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Immune System – KidsHealth

Wednesday, June 3rd, 2015

The immune system, which is made up of special cells, proteins, tissues, and organs, defends people against germs and microorganisms every day. In most cases, the immune system does a great job of keeping people healthy and preventing infections. But sometimes problems with the immune system can lead to illness and infection.

The immune system is the body's defense against infectious organisms and other invaders. Through a series of steps called the immune response, the immune system attacks organisms and substances that invade body systems and cause disease.

The immune system is made up of a network of cells, tissues, and organs that work together to protect the body. The cells involved are white blood cells, or leukocytes, which come in two basic types that combine to seek out and destroy disease-causing organisms or substances.

Leukocytes are produced or stored in many locations in the body, including the thymus, spleen, and bone marrow. For this reason, they're called the lymphoid organs. There are also clumps of lymphoid tissue throughout the body, primarily as lymph nodes, that house the leukocytes.

The leukocytes circulate through the body between the organs and nodes via lymphatic vessels and blood vessels. In this way, the immune system works in a coordinated manner to monitor the body for germs or substances that might cause problems.

The two basic types of leukocytes are:

A number of different cells are considered phagocytes. The most common type is the neutrophil, which primarily fights bacteria. If doctors are worried about a bacterial infection, they might order a blood test to see if a patient has an increased number of neutrophils triggered by the infection. Other types of phagocytes have their own jobs to make sure that the body responds appropriately to a specific type of invader.

The two kinds of lymphocytes are B lymphocytes and T lymphocytes. Lymphocytes start out in the bone marrow and either stay there and mature into B cells, or they leave for the thymus gland, where they mature into T cells. B lymphocytes and T lymphocytes have separate functions: B lymphocytes are like the body's military intelligence system, seeking out their targets and sending defenses to lock onto them. T cells are like the soldiers, destroying the invaders that the intelligence system has identified.

Here's how it works:

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Immune System - KidsHealth

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What Is the Immune System? (with pictures)

Monday, June 1st, 2015

Without it, we would all be forced to live in sterile environments, never touching each other, never feeling a spring breeze, never tasting rain. The immune system is that complex operation within our bodies that keeps us healthy and disease-free.

Few systems in nature are as complicated as the human immune system. It exists apart from, and works in concert with, every other system in the body. When it works, people stay healthy. When it malfunctions, terrible things happen.

The main component of the system is the lymphatic system. Small organs called lymph nodes help carry lymph fluid throughout the body. These nodes are located most prominently in the throat, armpit and groin. Lymph fluid contains lymphocytes and other white blood cells and circulates throughout the body.

The white blood cells are the main fighting soldiers in the body's immune system. They destroy foreign or diseased cells in an effort to clear them from the body. This is why a raised white blood cell count is often an indication of infection. The worse the infection, the more white blood cells the body sends out to fight it.

White and red blood cells are produced in the spongy tissue called bone marrow. This substance, rich in nutrients, is crucial for properly functioning immunity. Leukemia, a cancer of the bone marrow, causes greatly increased production of abnormal white blood cells and allows immature red blood cells to be released into the body. Other features, such as the lowly nose hair and mucus lining in the lungs, help trap bacteria before it gets into the bloodstream to cause an infection.

B cells and T cells are the main kinds of lymphocytes that attack foreign cells. B cells produce antibodies tailored to different cells at the command of the T cells, the regulators of the body's immune response. T cells also destroy diseased cells.

Many diseases that plague mankind are a result of insufficient immunity or inappropriate immune response. A cold, for instance, is caused by a virus. The body doesn't recognize some viruses as being harmful, so the T cell response is, "Pass, friend," and the sneezing begins.

Allergies are examples of inappropriate immune response. The body is hyper-vigilant, seeing that evil pollen as a dangerous invader instead of a harmless yellow powder. Other diseases, such as diabetes and AIDS, suppress the immune system, reducing the body's ability to fight infection.

Vaccines are vital in helping the body fend off certain diseases. The body is injected with a weakened or dead form of the virus or bacteria and produces the appropriate antibodies, giving complete protection against the full-strength form of the disease. This is the reason such disorders as diphtheria, mumps, tetanus and pertussis are so rarely seen today. Children have been vaccinated against them, and the immune system is on the alert. Vaccines have also been instrumental in eradicating plagues such as smallpox and polio.

Antibiotics help the body fight disease as well, but doctors are more cautious about prescribing the broad-spectrum variety, since certain bacteria are starting to show resistance to them. The next time you hug a loved one or smell a rose, thank your immune system.

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