Nieuws autoimmuunziekten


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Virus zendt ‘geheime’ boodschap tussen menselijke cellen

Nieuw ontdekt mechanisme belangrijk bij toekomstige behandeling kanker en auto-immuunziekten. Witte bloedcellen, geïnfecteerd met het Epstein Barr virus (o.a. ziekte van Pfeiffer), activeren afweercellen, zodat het virus niet gaat overheersen en de persoon gezond blijft. Dat gebeurt met een geheime boodschap die via minuscule blaasjes (exosomen) van de ene naar de andere cel worden overgebracht. Bij mensen met een ontregeld immuunsysteem slaat dit mechanisme juist op hol met chronische infecties tot gevolg.

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Stanfords onderzoek: immuunrespons op een griepeiwit verschaft nieuwe inzichten in narcolepsie

Een internationaal onderzoeksteam heeft voor het eerst substantieel bewijs gevonden dat erop kan duiden dat narcolepsie een “hit en run” auto-immuunziekte is. De onderzoekers hebben getracht vast te stellen waarom slechts een van de 2 verschillende griepvaccinaties toegepast tijdens de Mexicaanse grieppandemie in 2009 in verband werd gebracht met een sterke toename van narcolepsie, een zeldzame slaapstoornis.

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The Exploding Autoimmune Epidemic - Dr. Tent - It's Not Autoimmune, you have Viruses


Kwik in vis risicofactor voor auto-immuunziekte

Volgens een nieuwe studie aan de Universiteit van Michigan is één van de grootste risico's voor auto-immuniteit bij vrouwen in de vruchtbare leeftijd, de blootstelling aan kwik door het eten van schaal- en schelpdieren. Volgens de bevindingen, die gepubliceerd worden in Environmental Health Perspectives is er verband tussen het consumeren van kwik - op laag niveau in het algemeen als veilig beschouwd - en auto-immuniteit. Bijna 50 miljoen Amerikanen, voornamelijk vrouwen, lijden aan auto-immuunziekte waarbij het immuunsysteem per ongeluk gezonde cellen aanvalt.

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Darmbacteriën veroorzaken auto-immuunziekte op latere leeftijd bij muizen

Onderzoekers hebben ontdekt dat bij jonge muizen de kolonisatie van de darmen door bepaalde soorten bacteriën kan leiden tot immuun responses op latere leeftijd die verband houden met ziekte. Verhoging van niveaus van gesegmenteerde vezelige bacteriën kan veranderingen teweegbrengen in het lymfatisch weefsel van de muizendarmen, met als gevolg de productie van antilichaampjes die de componenten van de celkern aanvallen. Dit soort schade is kenmerkend voor auto-immuunziekten als systemische lupus erythematosus en systemische sclerosis waarbij organen in het gehele lichaam schade oplopen door willekeurige immuun responses.

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Wetenschappers ontdekken hoe je auto-immuunziekten ’uit kunt te schakelen'

Wetenschappers hebben een belangrijke doorbraak gemaakt in de strijd tegen slopende auto-immuunziekten zoals multiple sclerose, door te onthullen hoe cellen die gezond lichaamsweefsel aanvallen gestopt kunnen worden. In plaats van dat het immuunsysteem van het lichaam zijn eigen weefsel per ongeluk vernietigd, hebben onderzoekers van de Universiteit van Bristol ontdekt hoe cellen van agressief gedrag veranderen naar het daadwerkelijk beschermen tegen de ziekte. Men hoopt dat deze nieuwe inzichten leiden tot het wijdverbreide gebruik van antigeen-specifieke immunotherapie voor de behandeling van vele auto-immuunziekten als multiple sclerose (MS), diabetes type 1, de ziekte van Graves en systemische lupus erythematosus (SLE).

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The Exploding Autoimmune Epidemic - Dr. Tent - It's Not Autoimmune, you have Viruses


Plant 'fights auto-immune diseases'

Hydrangea, used for centuries in traditional Chinese medicine, may revolutionise the treatment for auto-immune diseases, it has been claimed.

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Stopping autoimmunity before it strikes

Current research describes a new method to track the development of autoimmune diseases before the onset of symptoms. The related report by Zangani et al, "Tracking early autoimmune disease by bioluminescent imaging of NF-?B activation reveals pathology in multiple organ systems," appears in the April 2009 issue of The American Journal of Pathology. Autoimmune diseases such as lupus, multiple sclerosis, rheumatoid arthritis and diabetes are caused when the immune system attacks the body's own cells. Normally, immune cells are prevented from attacking normal cells; however, in patients with autoimmune disease, this "tolerance" is lost. The immediate causes of autoimmune diseases remain unknown, partially due to the inability to detect disease before the onset of symptoms. Early detection of autoimmune disease is critical for assessing new treatments. The molecule NF-?B is activated by inflammation, which plays a key role in autoimmune disease development, making NF-?B a prime candidate to track autoimmune activity. Researchers at the University of Oslo led by Drs. Ludvig Munthe and Bjarne Bogen in collaboration with Rune Blomhoff engineered NF-?B such that it would emit light when activated. Using a mouse model of systemic autoimmunity with features of lupus, they found that NF-?B activation signals were present in affected organs several weeks before the clinical manifestations of disease. The light signal intensity correlated with disease progression. NF-?B tracking may therefore provide a new tool in the evaluation of early autoimmune therapies.

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New clue to machinery of autoimmune disease

St. Jude researchers have discovered an intriguing insight into how T cells, the immune system’s master regulatory cells, wage war on the body’s own tissues in such autoimmune disorders as multiple sclerosis, type 1 diabetes and rheumatoid arthritis. Their findings about T cells add another piece to the puzzle of understanding such diseases. While the findings are quite basic, they could contribute to designing therapies to suppress the immune responses that are misdirected against a person’s own tissues in autoimmune disorders.T cells launch the immune system into action when they encounter bits of foreign protein, called antigens. T cells sense these antigens—which may come from invading viruses or bacteria—through receptors on the T cells’ surface. These receptors recognize and attach to specific antigens like a key fitting a lock. Many autoimmune diseases arise when T cell receptors that recognize the body’s own proteins, called “self” antigens, spur T cells to mistakenly launch an immune system to attack body tissues.“T cells have potentially millions of different possible receptors,” said Terrence Geiger, MD, PhD, Pathology, the senior author of a report on this work that appears in the July 1 issue of the Journal of Immunology. “Some T cell receptors are adept at promoting autoimmunity, some are poor and some are protective. It is not clear why one T cell receptor can promote autoimmunity, whereas another T cell receptor on a similar kind of T cell either doesn’t do anything, or even protects against autoimmune reaction.”

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Vitamin A signals offer clues to treating autoimmunity

Distributed around the body, dendritic cells act as the security alarms of the immune system. After sensing the presence of intruders, dendritic cells can transmit the alarm to white blood cells or tell them to relax, depending on the signals they send out. Researchers at the Emory Vaccine Center and Yerkes National Primate Research Center have discovered that dendritic cells can respond to the same compound, through two different receptors, by sending out both stimulatory and calming messages at once. The compound is zymosan, a component of yeast cell walls. However, the finding could guide scientists in designing vaccines against many infectious agents since the calming receptor is known to respond to bacteria and viruses as well as yeast. In addition, silencing the calming receptor's messages might boost the immune system's ability to fight a chronic infection. The calming receptor, known as TLR2 (Toll-like receptor 2), uses vitamin A to transmit its signals, which provides an explanation for the connection between vitamin A deficiency and autoimmune diseases. Vitamin A deficiency has been linked to diseases such as rheumatoid arthritis, lupus and type I diabetes. This "two signals at once" feature of the immune system can be viewed as the result of an evolutionary tug of war, says senior author Bali Pulendran, PhD, professor of pathology and laboratory medicine at Emory University School of Medicine and Yerkes National Primate Research Center. "The immune system has to provide a defense against infection, while avoiding the destruction of too much of the body along the way," he says. "At the same time, pathogens have evolved strategies to manipulate the immune system for their own purposes."

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Neurotransmitter defect may trigger autoimmune disease

A potentially blinding neurological disorder, often confused with multiple sclerosis (MS), has now become a little less mysterious. A new study by researchers at the Mayo Clinic in Rochester, Minnesota, may have uncovered the cause of Devic's disease. Their new study, which will appear online on October 6th in the Journal of Experimental Medicine, could result in new treatment options for this devastating disease. Devic's disease, also known as neuromyelitis optica (NMO), results in MS-like demyelinating lesions along the optic nerves and spine. Affected individuals often experience rapid visual loss, paralysis, and loss of leg, bladder, and bowel sensation. Some lose their sight permanently. Unlike MS, Devic's disease can be diagnosed by the presence of a specific self-attacking immune protein—an autoantibody referred to as NMO-IgG—in the blood. Until now, however, clinicians didn't know how that protein damaged nerves and contributed to disease symptoms. The Mayo team, lead by Dr. Vanda Lennon, now show that NMO-IgG sets off a chain of events that leads to a toxic build-up of a neurotransmitter called glutamate. NMO-IgG binds to a protein that normally sops up excess glutamate from the space between brain cells. When NMO-IgG is around, this sponge-like action is blocked, allowing glutamate to accumulate. And too much glutamate can kill the cells that produce myelin—the protein that coats and protects neurons. The authors suggest that glutamate-induced damage to nerve cells and their insulating myelin coats might account for the neurological symptoms associated with Devic's disease. If the groups' results—generated using nerve cell cultures—are confirmed in vivo, drug development could be very straightforward. Therapeutic trials for glutamate blockers, created to treat other neurodegenerative diseases like Lou Gehrig's disease (or ALS), are already underway.

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Vitamin D may exacerbate autoimmune disease

Deficiency in vitamin D has been widely regarded as contributing to autoimmune disease, but a review appearing in Autoimmunity Reviews explains that low levels of vitamin D in patients with autoimmune disease may be a result rather than a cause of disease and that supplementing with vitamin D may actually exacerbate autoimmune disease. Authored by a team of researchers at the California-based non-profit Autoimmunity Research Foundation, the paper goes on to point out that molecular biologists have long known that the form of vitamin D derived from food and supplements, 25-hydroxyvitamin D (25-D), is a secosteroid rather than a vitamin. Like corticosteroid medications, vitamin D may provide short-term relief by lowering inflammation but may exacerbate disease symptoms over the long-term. The insights are based on molecular research showing that 25-D inactivates rather than activates its native receptor - the Vitamin D nuclear receptor or VDR. Once associated solely with calcium metabolism, the VDR is now known to transcribe at least 913 genes and largely control the innate immune response by expressing the bulk of the body's antimicrobial peptides, natural antimicrobials that target bacteria. Written under the guidance of professor Trevor Marshall of Murdoch University, Western Australia, the paper contends that 25-D's actions must be considered in light of recent research on the Human Microbiome. Such research shows that bacteria are far more pervasive than previously thought – 90% of cells in the body are estimated to be non-human – increasing the likelihood that autoimmune diseases are caused by persistent pathogens, many of which have yet to be named or have their DNA characterized. Marshall and team explain that by deactivating the VDR and subsequently the immune response, 25-D lowers the inflammation caused by many of these bacteria but allows them to spread more easily in the long-run. They outline how long-term harm caused by high levels of 25-D has been missed because the bacteria implicated in autoimmune disease grow very slowly. For example, a higher incidence in brain lesions, allergies, and atopy in response to vitamin D supplementation have been noted only after decades of supplementation with the secosteroid. Furthermore, low levels of 25-D are frequently noted in patients with autoimmune disease, leading to a current consensus that a deficiency of the secosteroid may contribute to the autoimmune disease process. However, Marshall and team explain that these low levels of 25-D are a result, rather than a cause, of the disease process. Indeed, Marshall's research shows that in autoimmune disease, 25-D levels are naturally down-regulated in response to VDR dysregulation by chronic pathogens. Under such circumstances, supplementation with extra vitamin D is not only counterproductive but harmful, as it slows the ability of the immune system to deal with such bacteria. The team points out the importance of examining alternate models of vitamin D metabolism. "Vitamin D is currently being recommended at historically unprecedented doses," states Amy Proal, one of the paper's co-authors. "Yet at the same time, the rate of nearly every autoimmune disease continues to escalate."

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Autoinflammatory disease model reveals role for innate, not adaptive, immunity

Researchers at the University of California, San Diego School of Medicine have developed the first mouse model for auto-inflammatory diseases, disorders that involve the over-activation of the body's innate, primitive immune system. Their study, published early on-line in Cell Immunity on June 4, suggests that the innate – not adaptive – immune system drives auto-inflammatory diseases. The findings could open new therapeutic directions for research into disorders such as gout or inflammatory bowel disease. "Auto-inflammatory diseases are a relatively new classification of diseases that are different from autoimmune diseases or allergies," said Hal Hoffman, MD, associate professor of medicine at UC San Diego School of Medicine. Hoffman studies a group of rare, inherited auto-inflammatory conditions called Cryopyrin-Associated Periodic Syndromes (CAPS), which includes Familial Cold Auto-inflammatory Syndrome (FCAS) and Muckle-Wells Syndrome (MWS). Autoimmune diseases arise from an overactive response of the body's adaptive, or acquired, immune system against substances and tissues normally present in the body. Allergies are also a product of the adaptive immune system, but in response to environmental substances. Both involve the action of lymphocytes such as B cells and T cells. The older innate immune system, on the other hand, recruits immune cells to sites of infection and inflammation, but doesn't confer long-time protection. Pathogens evoke an inappropriate response that doesn't involve antibodies or lymphocytes. With CAPS, Hoffman had earlier discovered that mutations of the NLRP3 gene caused the auto-inflammatory disease symptoms because the gene causes alterations in the protein called cryopyrin. Cryopyrin regulates the release of interleukin-1, an important mediator of fever and systemic inflammation during the body's innate immune response, and alterations in cryopyrin lead to over-production of Il-1. Mutations in the NLRP3 gene are thought to result in inappropriate activation of a multi-protein complex called an inflammasome, leading to excessive Il-1? release and manifestation of CAPS disease symptoms. Treatment with Il-1? inhibitors reduces the inflammation and symptoms in auto-inflammatory diseases; however, NLRP3 may have other effects in addition to increased Il-1?. "Patients treated with the Il-1? inhibitors got much better, but still exhibited some symptoms," said Hoffman.

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A new lead for autoimmune disease

A drug derived from the hydrangea root, used for centuries in traditional Chinese medicine, shows promise in treating autoimmune disorders, report researchers from the Program in Cellular and Molecular Medicine and the Immune Disease Institute at Children's Hospital Boston (PCMM/IDI), along with the Harvard School of Dental Medicine. In the June 5 edition of Science, they show that a small-molecule compound known as halofuginone inhibits the development of Th17 cells, immune cells recently recognized as important players in autoimmune disease, without altering other kinds of T cells involved in normal immune function. They further demonstrate that halofuginone reduces disease pathology in a mouse model of autoimmunity. Currently there is no good treatment for autoimmune disorders; the challenge has been suppressing inflammatory attacks by the immune system on body tissues without generally suppressing immune function (thereby increasing risk of infections). The main treatment is antibodies that neutralize cytokines, chemical messengers produced by T cells that regulate immune function and inflammatory responses. However, antibodies are expensive, must be given intravenously and don't address the root cause of disease, simply sopping up cytokines rather than stopping their production; patients must therefore receive frequent intravenous infusions to keep inflammation in check. Powerful immune-suppressing drugs are sometimes used as a last resort, but patients are left at risk for life-threatening infections and other serious side effects. Through a series of experiments, the researchers show that halofuginone prevents the development of Th17 cells in both mice and humans, halts the disease process they trigger, and is selective in its effects. It also has the potential to be taken orally. "This is really the first description of a small molecule that interferes with autoimmune pathology but is not a general immune suppressant," says Mark Sundrud, PhD, of the PCMM/IDI, the study's first author.

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Stopping Autoimmunity Before It Strikes

Current research describes a new method to track the development of autoimmune diseases before the onset of symptoms. The related report by Zangani et al, “Tracking early autoimmune disease by bioluminescent imaging of NF-?B activation reveals pathology in multiple organ systems,” appears in the April 2009 issue of The American Journal of Pathology. Autoimmune diseases such as lupus, multiple sclerosis, rheumatoid arthritis and diabetes are caused when the immune system attacks the body’s own cells. Normally, immune cells are prevented from attacking normal cells; however, in patients with autoimmune disease, this “tolerance” is lost. The immediate causes of autoimmune diseases remain unknown, partially due to the inability to detect disease before the onset of symptoms. Early detection of autoimmune disease is critical for assessing new treatments.

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'Autoantibodies' may be created in response to bacterial DNA

Autoimmune diseases have long been regarded as illnesses in which the immune system creates autoantibodies to attack the body itself. But, researchers at the California non-profit Autoimmunity Research Foundation (ARF) explain that the antibodies observed in autoimmune disease actually result from alteration of human genes and gene products by hidden bacteria. Not long ago, scientists believed they had located all bacteria capable of causing human disease, But DNA discoveries in the last decade have led the NIH Human Microbiome Project to now estimate that as many as 90% of cells in the body are bacterial in origin. Many of these bacteria, which have yet to be named and characterized, have been implicated in the progression of autoimmune disease. In a paper published in Autoimmunity Reviews, the ARF team, under the guidance of Professor Trevor Marshall of Murdoch University, Western Australia, has explained how Homo sapiens must now be viewed as a superorganism in which a plethora of bacterial genomes – a metagenome – work in concert with our own. Marshall and team contend that the human genome can no longer be studied in isolation. "When analyzing a genetic pathway, we must study how bacterial and human genes interact, in order to fully understand any process related to the human superorganism," states Marshall. "Especially since some of these pathways contribute to the pathogenesis of autoimmune disease." For example, the team notes that the single gene ACE has an impact on myocardial infarction, renal tubular dysgenesis, Alzheimer's, the progression of SARS, diabetes mellitus, and sarcoidosis, yet recently ACE has been shown to be affected by the common species Lactobacillus and Bifidobacteria. Found in yogurt, these species are often considered to be innocuous or "friendly." "No one would argue that these species aren't present in the human body, yet there has been inadequate study of how these 'friendly' species affect disease," states Amy Proal, the paper's lead author. "What we thought were autoantibodies generated against the body itself can now be understood as antibodies directed against the hidden bacteria," states Marshall. "In autoimmune disease, the immune system is not attacking itself. It is protecting the body from pathogens."

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New protein discovery helps researchers understand autoimmune diseases

APS-1 is an rare hereditary disease where the immune system attacks the body's own organs. Within the framework of a major EU project, coordinated by Professor Olle Kämpe at Uppsala university, scientists have now managed to identify a protein that opens new possibilities of understanding both APS-1 and other autoimmune disorders. The discovery is being published in the American journal The New England Journal of Medicine.

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The Paleolithic Diet

Some researchers believe that Neolithic foods - the foods introduced into the human diet at the start of the Neolithic Era - are the cause of autoimmune disease. Loren Cordain's articles give details of the mechanism. The book NeanderThin is a case in point - written by someone with multiple autoimmune disease who was healed by a paleolithic diet.

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Potential autoimmunity-inducing cells found in healthy adults

It's not just patients with autoimmune diseases like lupus and rheumatoid arthritis (RA) that have self-attacking immune cells—healthy people have them too, according to a new report in the Journal of Experimental Medicine. In healthy adults, however, these cells are maintained in an 'off' state, perhaps explaining their innocuous nature. Whether these cells are the true predecessors of the self-attacking cells prevalent in lupus and RA and, if so, what prevents them from causing disease in everyone is not yet known. The new study will appear online on December 22nd. As antibody-producing B cells develop in the bone marrow, the body tests them to determine whether their antigen receptors are apt to confuse self tissues for intruders. If so, their receptors are either rearranged to make new, non-autoreactive versions—a process called 'receptor editing'—or the cells are killed off while still in the bone marrow. Yet a minority manages to escape, slipping into the body as mature B cells with a propensity for self-attack.

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Unexpected finding opens up new way to stop autoimmune diseases and transplant rejection

After several years of battling recurring infections, the last thing a patient and her doctors ever expected was that the cause of her problems might actually help millions live longer, more active lives. Now, researchers have high hopes because Edward Goetzl and his colleagues from the University of California and The Ohio State University discovered that the patient made a unique antibody to her own T cells, the cells that mediate much of autoimmunity. Acting on the surface of T cells via a novel mechanism, the antibody reduced the number of T cells in her blood stream: a result that usually requires a host of "immunosuppressive" and possibly toxic drugs. Their research discovery, published online in The FASEB Journal, may lead to entirely new therapies for a wide range of autoimmune disorders, such as colitis, lupus, rheumatoid arthritis, inflammatory bowel disease, and multiple sclerosis, as well as new ways to prevent transplant rejection."The possibility that these antibodies can be used to treat diverse autoimmune diseases with minimal risk of infections represents a new horizon for reversing these disabling and often fatal conditions," said Edward Goetzl, a senior researcher involved in the study.

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UCSF finds potential new antibody treatment for autoimmune diseases

Scientists at UCSF have discovered an abnormality in a patient’s immune system that may lead to safer therapies for autoimmune diseases such as rheumatoid arthritis and colitis, as well as potential new ways to treat transplant rejection. The research identified antibodies from a woman’s immune system that prevent infection-fighting T cells from moving through her blood stream and entering her body’s organs to attack invaders such as bacteria or viruses. Findings appear in the current online edition of “The FASEB Journal,” the official journal of the Federation of American Societies for Experimental Biology. Based on studies in which the woman’s antibodies were transferred into mice, researchers hope these antibodies can be used to treat patients with autoimmunity or transplant recipients whose immune systems attack a transplanted organ or tissue. Autoimmunity occurs when the body perceives its own cells or tissue as foreign organisms and creates an immune response to itself. Autoimmune diseases affect approximately five to eight percent of Americans and their prevalence is increasing, according to the National Institute of Allergy and Infectious Diseases. The majority of people with autoimmune diseases are women.

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autoimmuunziektes
The Marshall protocol

Th1 inflammatory diseases are characterized by the generation of Interferon-gamma and with it, 1,25-dihydroxyvitamin-D in response to intracellular bacteria. We are researching which diseases show scientific evidence that they are due to a Th1 immune system inflammatory response. There are hundreds of so-called 'autoimmune' diseases. Autoimmune is a misnomer since the body's immune system is not attacking itself. We use this term only because it is familiar and easily recognizable not because it is accurate. Many common diseases like atherosclerosis are being recognised as having an inflammatory component. We can make an educated guess about which diseases would be more difficult to treat with the MP because the symptom exacerbation might be difficult to manage.

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autoimmuunziektes
What is the Marshall Protocol?

The Marshall Protocol is a curative treatment for diseases having a TH1 type immune response. Patients having been diagnosed with one or more of a wide range of diseases have been successfully treated using this protocol. It works by enabling the immune system to destroy the intracellular bacteria that are thought to be the root cause of the illness.

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CureMyTh1.org

CureMyTh1.org is moderated by folks with Th1 inflammatory disease who are being treated with the Marshall Protocol (MP). They do not have medical expertise but are knowledgeable about the disease process and the MP. They are eager to answer your basic questions so you can decide if you would like to participate in the clinical study of the Marshall Protocol.

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The marshall protocol - Phase 1

Professor Trevor G. Marshall began studying chronic disease at the University of Western Australia in 1978, with a focus on diabetes, infertility, and sarcoidosis. At the turn of the 21st Century, he identified the pathogenesis of the Th1 immune system response — an antibiotic-resistant, intra-phagocytic, metagenomic microbiota, consisting primarily of pleomorphic, cell-wall-deficient (CWD) bacteria [1]. Tools of modern molecular genomics enabled Dr. Marshall to develop an antibacterial protocol which stimulates innate immunity at the same time as it weakens this metagenomic microbiota. The Phase II clinical trial conducted by the Autoimmunity Research Foundation has demonstrated applicability of this antibacterial therapy to a wide range of chronic Th1 immune illnesses [2]. This confirms Dr. Marshall’s prediction that most chronic disease springs from genomic variations of the same fundamental mix of relatively common pathogens.

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The marshall protocol - Phase 2

The Marshalls’ paper "Antibiotics in Sarcoidosis" [1] states that there are many different species of Cell Wall Deficient (CWD) bacteria which can contribute to Th1 inflammation. It has become clear that low dose, pulsed Minocycline (Mino) used in Phase One of the MP, while very effective, does not eliminate all the species of intra-phagocytic bacteria needed to effect a cure. After exhaustive research, the Marshalls have identified several other antibiotics which work by exerting a complimentary blockade of bacterial-protein synthesis. When these antibiotics are taken along with Mino (at low-dose, pulsed intervals), they are far more effective than if they were taken alone. Benicar, taken 40mg every six hours both provides an inflammatory blockade and re-activates the VDR Nuclear Receptor.

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Scientists find new structural motif in key enzymes is essential to prevent autoimmune disease

Scientists from the Scripps Research Institute and the Genomics Institute of the Novartis Research Foundation have found a specific mutation that leads to the development of severe autoimmune kidney disease in mice. The research sheds light on the basic biology of the immune system, as well as on the effectiveness of drugs such as the anti-leukemia medication Gleevec/Imatinib. The study was published in the January 16, 2009 edition (Volume 33, No. 1) of the journal Molecular Cell. In the study, the scientists identify a disease-causing mutation in a binding structure common to dozens of kinases—specific enzymes, especially important in cell signaling, that can modify other proteins by transferring a phosphate group onto them. The mutation reduced the activity of an important kinase, Lyn (a member of the Src family, which modulates important cellular processes including cell migration, proliferation, and differentiation). "Our study has several important implications," said Karsten Sauer, a Scripps Research scientist and assistant professor who led the study. "First, it shows that when you eliminate the activity of the Lyn kinase through mutation, you develop problems in B cell signaling, resulting in B cell hyperactivity which leads to a severe autoimmune reaction—in this case, autoimmune glomerulonephritis, a form of kidney disease very similar to human lupus. This shows for first time how essential the Lyn kinase activity, and not potential adaptor or scaffold functions of the protein, is for B cell signaling, and for preventing autoimmune disease." B cells produce pathogen-fighting antibodies and are a critical part of the adaptive immune system.

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Autoimmunity Research Foundation

The Autoimmunity Research Foundation is a 501(c)3 charity whose educational efforts are focused on letting Health Professionals, and the public, know the putative cause of Th1 chronic inflammatory disease. Many chronic conditions, including Sarcoidosis, RA, MS, PTLDS, Chronic Fatigue Syndrome CFS/ME, Fibromyalgia, and Parkinson's, are succumbing to treatments based on our molecular description of inflammatory disease biology.

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