Category Archives: immune system

Arthritis and Your Diet: New Research Part 6


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There is some scientific reasons to think that diet effects arthritis and diet may serve as a risk factor by increasing your chances for developing certain kinds of arthritis. Diet may also change the way the body’s defenses, the immune system reacts in certain kinds of arthritis that involve inflammation and inflammation is a part of the body’s defense system. It can cause the swelling, redness, warmth and tenderness that come with some kinds of arthritis.

How diet affects the response of the immune system is a central question in several research studies. These studies are looking at the role of diet in worsening or lessening symptoms in certain types of arthritis. This topic will be addressed at a later date in more depth.

There are some very early studies in animals and in small numbers of people with certain types of arthritis suggest, but doesn’t prove, that changes in diet may help. The results of these studies are experimental and need to be studied further in large numbers of people. There really isn’t enough scientific facts to recommend to people with arthritis any of the dietary changes except in weight control. However, I made some diet changes and got great results. I eliminated processed foods or pre-packaged foods and sugar from my diet and added more fresh fruits and vegetables and my arthritis symptoms were reduced. So, I do know that diet changes can make a difference.

Your weight and osteoarthritis:

Being very overweight or obese increases your risk for developing osteoarthritis in the knees. Those who are overweight tend to develop osteoarthritis in the knees at an earlier age than people with ideal weights for their heights. Weight is only one of several factors that increase your chances for osteoarthritis in the knees.

Food Allergies/Reactions:

Reactions to certain foods by the immune system may lead to or worsen symptoms in certain kinds of arthritis and researchers think it’s possible that a few otherwise healthy people develop temporary symptoms of arthritis from an allergic reaction to food. In a few people who already have arthritis, reactions to certain foods ma worsen symptoms. However, there have been observations that suggest that for most people who thought their arthritis symptoms were related to food, a connection between food and their arthritis symptoms couldn’t be confirmed.

Fasting/Low Calorie/ Low Fat Diets:

The immune system may work to lessen symptoms in response to other factors in your diet. There have been several researchers who have observed that fasting and low-calorie/low-fat/low protein diets could slightly reduce some symptoms of rheumatoid arthritis in humans or lupus in animals. Scientists don’t yet understand why this happens or if certain changes in diet, such as short-term fasts, help.

Fatty Acids/Fish Oils:

Another example of the possible effects of diet on arthritis is the role of certain fatty acids in the chemical chain reaction that causes inflammation. Just for instance, oils from some cold water fish and plants block the body from making certain chemicals.

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Discovery Could Change The Way Your Doctor Treats Your Autoimmune Disease or Cancer


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Researchers in the Faculty of Medicine & Dentistry at the University of Alberta have an important discovery that provides a new understanding of how our immune system “learns” not to attack our own body, and this could affect the way doctors treat patients with autoimmune diseases and cancer.

When patients undergo chemotherapy for cancer or as part of experimental therapies to treat autoimmune diseases such as diabetes and lupus, the treatment kills the patients’ white blood . What can be done afterwards, is to give these patients blood stem cells through transplantation. Stem cells taken from patients then injected back into them – with the theory being that the patients’ immune system won’t attack their own cells, and the  can get to work healing their bodies.
But U of A medical researchers Govindarajan Thangavelu, Colin Anderson and their collaborators discovered that if a particular molecule is not working properly in T-cells, the body will attack itself. This is significant for stem-cell transplantation treatment because it means the immune systems of the patients could consider their own cells “foreign” and start an attack.
“So your own cells would be killing you,” says Thangavelu, a PhD student specializing in immunology, who was the first author in the research study, which was recently published in the peer-reviewed Journal of Auto-immunity. “What we found is if this molecule is absent in T-cells, if the pathway isn’t intact, it will cause severe auto-immunity to the subject’s own body. In essence, subjects become allergic to their own cells.”
Anderson, an associate professor with the Alberta Diabetes Institute and Principal Investigator added: “The ability of our immune system to attack dangerous microbes while not attacking our own cells or tissues is a delicate balance. Restarting the immune system after wiping it out in patients with autoimmune diseases or cancer requires re-establishing this proper balance. We discovered that a particular immune system molecule is critical to prevent the immune system from attacking our own cells or tissues when the immune system is restarted. If that molecule is missing, the  will wreak havoc on the body.”
T-cells are supposed to protect people and animals from things invading their bodies. But this research demonstrates if these cells become unregulated because they are missing a molecule, it can lead to auto-immunity – particularly dangerous in scenarios where patients have lost white blood cells when being treated for  or cancer.
Thangavelu has won awards for this research.  He was invited to present his work at an international conference of immunology in Japan last year. He has also travelled to the United Kingdom to talk about his findings with the medical community.
Provided by University of Alberta (news : web)

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Attention: Scientists Discover ‘How to Stop Your Immune System From Killing You’


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>(Medical Xpress) — Scientists at the University of Birmingham have discovered a ‘molecular hover’ with the potential to prevent autoimmune conditions.
Research findings published today in the journal Science by Dr David Sansom and his team in the MRC Centre for Immune Regulation at Birmingham show how a , called CTLA-4, keeps the  damped down during day-to-day activities and prevents inappropriate aggressive behaviour from T cells, the ‘command centre of our immune response’.

‘Only when we are truly infected with invading microbes is the alarm system allowed to work properly, unleashing the full force of our immune system in the right place and at the correct time,’ says Dr Sansom.
‘We all take our immune system for granted,’ he explains. ‘Every day we are faced with a constant barrage of infectious agents just dying to make our bodies their home. To prevent this invasion, our immune system deploys a range of weapons designed to eat, poison and ultimately kill unwanted and potentially dangerous guests. On the whole, the immune system is remarkably good at its job.’
Why does this potent arsenal of weapons not kill us? ‘The fact is that a number of diseases can be caused by such collateral immune damage, indeed rheumatoid arthritis, Type 1 diabetes and inflammatory bowel syndrome are all thought to be examples of  where the immune system attacks our bodies in some way,’ says Dr Sansom.
One essential part of our immune system is CTLA-4, a protein found on T cells, he says. ‘Without CTLA-4  start to recognise our bodies, leading to the attack of many organs in a way which is fatal.’
While immunologists have known for a long time that CTLA-4 is required to prevent immune responses against ourselves, how it works has remained a mystery. The Sansom lab’s work puts in place a critical piece of the puzzle by illustrating that CTLA-4 acts as a Hoover removing the alarm signals that can drive unwanted and damaging immune responses against our bodies.
The work was funded by the Biotechnology and Biological Sciences Research Council (BBSRC) and the findings provide a new way of thinking about how to gain better control of our immune response and may help in the design of drugs to treat autoimmune diseases such as arthritis and diabetes.
Dr Sansom adds: ‘Alternatively, by discovering new ways to prevent CTLA-4 working, it may be possible to encourage our immune cells to attack cells of our own bodies which could be desirable in cancers.’
In either case, he says, understanding how CTLA-4 works and learning how to manipulate its behaviour represents a significant step in understanding self-control in the immune system.

Provided by University of Birmingham

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First Breakthrough in 50 Years For Lupus


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(Medical Xpress) — A Monash researcher has played a crucial role in the first major lupus treatment breakthrough for over 50 years.

Professor Fabienne Mackay Head of the Department of  at Monash University, discovered a new factor in the development of the disease, something known as BAFF – B cell Activating Factor.

It has led directly to the development of a medication called Benlysta, which was approved by the US Food and Drug Authority for release last month.
Professor Mackay explains that B  make  for invaders such as  and other foreign bodies, like pollen.
“BAFF helps B cells survive, which is a good thing. But if there is too much BAFF, then there can be an overproduction of B cells and they hang about for longer than they should – in particular  that are normally meant to die because they are harmful. Auto-immunity will be initiated, and this is how the immune system ends up attacking the body’s own cells,” Professor Mackay said.
Lupus is an autoimmune inflammatory disease affecting about five million people worldwide. An autoimmune problem is one where the body’s immune system attacks the body itself.  In the case of lupus, the  attacks connective tissue in the joints, lungs, kidneys and heart, causing joint and skin diseases in most patients, and organ and blood disorders in about half of lupus sufferers.
Professor Mackay was the first to show that the overproduction of BAFF was driving lupus. In a follow-up study, elevated levels of BAFF were discovered in patients with a number of autoimmune diseases including lupus, rheumatoid arthritis and Sjögren’s syndrome.
She said this was an exciting discovery as it implied that if BAFF production can be blocked, the entire cascade effect that resulted in autoimmune disease could be prevented.
Manufacturers of the drug, GlaxoSmithKline designed their clinical trials in line with the insights from Professor Mackay’s experimental data.
Professor Mackay says that one of the reasons for her interest in lupus is its effect on the Indigenous Australian population. Aboriginal Australians suffers from  at a rate double that of the non-Aboriginal population.
“I am very pleased to have created the platform of knowledge from which effective therapies can springboard. In particular, I have long been concerned about the higher incidence of this disease and associated morbidity within Indigenous Australians populations and the limited arsenal of therapies, many very toxic, and it is wonderful news that a medication has been developed which may be able to help them.”
Provided by Monash University (news : web)

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The New Structure of An Important Immune System Complex Has Resolved A 10-year Controversy


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(Medical Xpress) — Researchers at the University of Toronto and the University of Bath have resolved a longstanding controversy surrounding an important structure of the immune system that could result in new therapeutic targets for antibody-mediated autoimmune diseases as well as the potential to enhance the efficacy of vaccines.

In a study published in the April 29 issue of Science, Professor David Isenman of biochemistry and Jean van den Elsen of the University of Bath shed light on the complex between complement receptor 2 and its  C3d, both of which are constituents of an  of our body known as complement.

“We recognize that the goal of applying this knowledge to autoimmune therapies and enhanced vaccine efficiency will not be trivial. But the structural scaffold for further discoveries is now in place,” said Isenman.
The detailed knowledge of the receptor-ligand interface provided by the new structure of this complex has implications as both a potential , in the case of antibody-mediated , and as something that may be exploited in enhancing the efficacy of vaccines.
The role of complements in mediating the clearance of microbial pathogens, either directly or in conjunction with , has long been recognized. A key element of the process is the “tagging” of the foreign target by a proteolytically activated fragment of complement part C3. This first C3 split product, as well as its next degradation products, remains covalently attached to the foreign target where they act as ligands (i.e., bridging molecules) for complement receptors present on white blood cells. In turn, these white blood cells can engulf and destroy the tagged microbial target.
New structure of an important immune system complex resolves a 10-year controversy
In more recent years, it has become well established that complement also plays a role in focusing the antibody arm of the adaptive  on an antigen which it has tagged with a C3 split product, the limit one of which is known as C3d. The latter is a ligand for complement receptor 2 (CR2) on B lymphocytes, the very type of cell that, when stimulated by a specific antigen, undergoes clonal expansion and ultimately differentiates into “factory” cells that secrete large amounts of the antibody against the antigen that was initially met. As illustrated in the accompanying schematic, both the antigen recognition entity of the B cell (the B cell receptor, BCR), as well as the C3d-binding CR2 molecule, are each associated with other molecules involved in generating intracellular signals that drive B cell clonal expansion. In what is known as the co-ligation model, the C3d-tagged antigen mediates a bridge between the BCR complex and the CR2/CD19/CD81 complex, the effect of which is to greatly enhance the amount of signalling on that achieved by antigen binding to the BCR alone. What this does is lower by orders of size the threshold measure of antigen required to start the antibody response of the particular B cell recognizing that particular antigen. There is an extra role for CR2 present on a different cell type, the follicular dendritic cell (FDC) of lymph nodes, in trapping C3d-tagged antigen in the lymph node. This in turn is important in generating stronger binding antibodies and in the induction of long-lived memory B cells that allows one to rapidly mount an antibody response years after the first encounter with a particular antigen. These effects, which are mediated by the CR2-C3d interactions on B cells and FDCs, are collectively called the “molecular adjuvant” effects of complement and this is important in making the antibody response sensitive to the low concentrations of antigen that are present in the early stages of infection. Unfortunately, these same CR2-C3d binding events can sometimes lead to harmful effects in the case of people having B cells that are reactive against self-antigens and which produce the antibodies at the root of antibody-mediated autoimmune diseases such as systemic lupus erythematosus (commonly known as lupus disease or SLE).
Clearly there is a potential to therapeutically exploit the CR2-C3d interaction, either through the rational design of drugs that would inhibit the interaction in the case of some autoimmune conditions or the rational design of small molecule CR2-binding memetics of C3d, which may be used to decorate antigens in a subunit (i.e,. pathogen surface protein-based, as opposed to whole pathogenic microorganism-based)  situation. Unfortunately, the molecular details of the CR2-C3d interface (represented within the white box of the schematic) necessary to pursue such therapeutic avenues have been mired in controversy for the past decade. Specifically, in 2001 an X-ray crystal structure of the complex consisting of C3d and the first two domains of CR2 [hereinafter denoted CR2(SCR1-2)] was published in Science, however from the start that structure was discordant with much biochemical data in the literature, and over the years the discrepancies have only increased.
“To be clear, there were no errors made in the original structure determination, but it is now clear from extensive subsequent biochemical work that the 2001 structure represented a non-physiologic complex that resulted from the particular crystallization conditions used,” said van den Elsen.
The structure of the CR2(SCR1-2)-C3d complex from van den Elsen and Isenman was also determined using X-ray crystallography, but under more physiologic crystallization conditions. The new structure (depicted here) is very different from the previous one, but its features do conform to all existing biochemical data. With the controversy regarding atomic level details of the binding interface now finally resolved, the new structure of the CR2(SCR1-2)-C3d complex will hopefully provide the platform for both the design of compounds that may exploit this interface as either a therapeutic target or in enhancing the efficacy of vaccines. While this discovery lays an important foundation, the authors of the current study recognize that neither of these goals will be simple to achieve and will require contributions from medicinal chemists, in addition to complementologists and immunologists.
Provided by University of Toronto (news : web)

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>Natural immune modulators may provide a key to beating immune disorders


>Natural immune modulators may provide a key to beating immune disorders

(NaturalNews) The immune system is normally our natural first line of defense against illness and bad health. However, sometimes immune systems function abnormally due to deficiencies and disorders where the body either loses its natural immunity or else the immune system turns against the body it is supposed to protect. In either case, natural immune modulators may provide the key to maintaining a strong and properly functioning immune system.

Immunodeficiency (or immune deficiency) is a state in which the immune system’s ability to fight infectious disease is compromised or entirely absent. There are more than 80 different immune-deficiency syndromes, including the most common and well-known immune deficiency, AIDS (Acquired Immune Deficiency Syndrome).

Mainstream medicine has little understanding and no cure for immunodeficiency and often attempts to manage it through long-term antibiotics. Antibiotics often have dangerous side effects. In addition, long term use of antibiotics destroys the body’s beneficial intestinal bacteria which leads to bacterial overgrowth, lowered digestion and absorption of nutrients and ultimately even lower natural immune function.

Autoimmune disorder is a condition that occurs when the immune system mistakenly attacks and destroys healthy body tissue due to an inability to distinguish between healthy body tissue and antigens (such as microbial pathogens). The result is an immune response that destroys normal body tissues.

As is the case with immunodeficiencies, mainstream medicine has little understanding and no cures for autoimmune disorders. In most instances, mainstream medicine employs unnatural immunosuppressive drugs to reduce the immune system response. Besides a number of dangerous side effects such drugs often cause, they also reduce the body’s natural immune response to actual illness.

Nature may provide a key for controlling and beating immune disorders in the form of natural immune modulators. Immune modulators can either up-regulate or down-regulate natural immune response as needed, enabling people with immune disorders to have more normalized immune function without the side effects of unnatural medications.

Five powerful natural immune modulators are:

Magnesium

Magnesium is a powerful and essential immune modulator. Known as the “master mineral”, magnesium is involved in no fewer than 300 body processes. A deficiency in magnesium has been strongly linked to immune disorders and it has been variously estimated that anywhere from 70 to 95 percent of us are deficient in magnesium.

Vitamin D3

Vitamin D3, known as the “sunshine vitamin”, is essential to life itself. Several studies in recent years have indicated that vitamin D3 is a powerful immune modulator which could be useful against autoimmune disorders. Furthermore, like magnesium, deficiency in D3 has been linked to autoimmune disorders. The best source of D3 is sunshine. When that is not feasible, supplemental D3 can help.

Curcumin

Curcumin is the major component of the common kitchen spice “turmeric”. It is a wonderful herb which has anti-inflammatory and anti-cancer properties and it has been shown to inhibit autoimmune disorders. Note: curcumin is ordinarily not very bio-available. Consuming piperine (black pepper) and/or coconut milk may improve absorption somewhat, but the best therapeutic value may be found in curcumin supplements designed for high bio-availability.

Blackseed oil

Blackseed oil (Nigella sativa) is another powerful immunomodulator and it has been used for centuries for a wide variety of illnesses. The prophet Muhammad was reported to have said that blackseed is a “cure for everything but death”.

Oleander extract

Oleander is noted as a supreme immune stimulator and for its success against cancer, HIV and other conditions. However, it appears that oleander is also a powerful immune-modulator, with many reports of it helping people with immune disorders. Note: only properly prepared non-toxic supplemental oleander extract should be used since the raw plant is quite toxic.

Sources included:

http://en.wikipedia.org/wiki/Immuno…
http://www.ncbi.nlm.nih.gov/pubmed/…
http://www.sclerodermatt.org/articl…
http://www.naturalnews.com/029804_s…
http://www.nationaljewish.org/healt…
http://www.ncbi.nlm.nih.gov/pubmed/…
http://www.islamicboard.com/health-…

Learn more:http://www.naturalnews.com/032121_immune_modulators_disorders.html#ixzz1K0CwZSTX

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>Conclusion On Natural Approach For Chronic Joint Pain & Inflammation — Anti-Aging Barron Report


>A Five-Pronged Natural Approach For Chronic Joint Pain & Inflammation — Anti-Aging Barron Report


Conclusion on Chronic Joint Pain

This formula now offers a five pronged approach to systemically relieving chronic joint pain and inflammation.
  1. It incorporates ASU to increase aggrecan levels, thereby helping to repair and rebuild damaged cartilage in the weight bearing joints.
  2. It makes use of the unique ability of the undenatured type II chicken collagen found in UC-II™ to train the body’s immune system to stop attacking joint cartilage.
  3. It makes use of ginger’s ability to directly reduce pain and inflammation.
  4. It makes use of CMO’s ability to lubricate joints, to support the rebuilding of cartilage, and stop the immune system from attacking joint tissue.
  5. And it makes use of the ability of 5-LOXIN to control inflammation.

Things To Take With this Formula

Immune boosters and pathogen destroyers. Once again, the “scientific community” is years late in acknowledging the commonly known fact that, in most cases, joint pain is related to a compromised immune system. Take rheumatoid arthritis, for example. The Journal of Clinical Pathology has finally endorsed what the Mayo Clinic demonstrated conclusively years ago: that bacteria are involved. And new research is indicating that mycoplasma infections may be responsible for as much as 50% of all chronic disease, including arthritis.
Glucosamine and chondrotin sulfate are not a cure, but for some people 1,000-2,000 mg a day may provide some relief. Studies are decidedly mixed, but if it works for you, that’s all that counts.
Systemic proteolytic enzymes can be remarkably effective in reducing inflammation throughout the body. Reducing the imflammation can go a long way in stopping the damage from progressing any further — in addition to reducing the pain.
Omega-3 fatty acids as found in fish and krill oil are also helpful in reducing inflammation.
MSM is a naturally occurring sulfur compound found in our bodies and in many foods. When taken as a supplement, it can play a major role in reducing joint inflammation.

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>Five simple eating principles your body is dying to follow


>Five simple eating principles your body is dying to follow

(NaturalNews) There are several basic principles of health that your body is dying to follow. Here is a brief discussion of 5 of these, as they pertain to eating, below. If we follow these principles we can be assured of great benefits because indeed an ounce of prevention is worth a pound of cure.

Regularity In Meals

First let’s look at regularity in meals. It is ideal to maintain a regular schedule not eating too late or eating at irregular times. By eating at the same time daily, the stomach will get used to eating at a certain time each day. This will encourage rhythm within the stomach. This will facilitate the entire gastrointestinal tract. Many people set the stage for gastrointestinal problems by eating and drinking at irregular times.

Learn more:http://www.naturalnews.com/030812_eating_body.html#ixzz18w9KlaKG

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Immune cell plays unexpected role in autoimmune disease


A new study provides fascinating insight into the underlying pathology associated with the autoimmune disease, systemic lupus erythematosus (SLE).  The research, published by Cell Press in the December issue of the journal Immunity, reveals an unexpected role for a key type of immune cell and provides a potential new therapeutic strategy for SLE and, potentially, other autoimmune diseases.

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>Reishi Mushrooms Offer Help For Those With Rheumatoid Arthritis


>One of the key measures of a long and well lived life is adaptability.  A person’s ability to adapt to changing circumstances goes a long way toward predicting longevity.  This involves the responsiveness and functionality of the immune system.  A robust immune system capable of adjusting to ever-changing situations is a key factor in preventing the manifestation of a cold or cancer, or anything inbetween.  One important aspect of immune function is its ability to self-regulate downward when needed so that it doesn’t become hyperactive and attact your own tissues, as in the case with Rheumatoid arthritis.  Read More

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