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Multiple Sclerosis: Back to Basics

Discussion in 'General Issues and Discussion Forum' started by NewsBot, Jun 3, 2013.

  1. NewsBot

    NewsBot The Admin that posts the news.

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    Press Release:
    Multiple sclerosis: Back to basics?
    Link to article: http://f1000.com/prime/reports/m/5/20/
     
  2. Admin2

    Admin2 Administrator Staff Member

  3. Mr C.W.Kerans

    Mr C.W.Kerans Active Member

    I had an unfortunate female patient who had rapidly progressive MS, with severe muscle spasm who in consequence had trouble with an IGTN - ingrown toenail - (left 1st). She went on to develop leukaemia, and while in hospital for chemotherapy, she developed an acute IGTN. The dilemma faced was if the IGTN was not remedied, and her compromised immune system led to infection, her chemo schedule would have been interupted. If need arose to use LA in treating the ingrown toenail, nobody could advise me if the LA would be effective - I still don't know. In the event, conservative measures were successful; she sadly died from the leukaemia. Does anybody have any views on this unusual situation?
     
  4. NewsBot

    NewsBot The Admin that posts the news.

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    Press Release:
    MS Treatment Options Growing, Raising New Hope, Loyola Neurologist Reports
    'Rapid expansion' of medications for Multiple Scerlosis
     
  5. NewsBot

    NewsBot The Admin that posts the news.

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    Press Release:
    First study to investigate the human genome in multiple sclerosis
    The National Institutes of Health awarded Benaroya Research Institute at Virginia Mason $1.9 million to find marks in the human genome which can explain why some white blood cells cause damage to the spinal cord and brain in multiple sclerosis
     
  6. NewsBot

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    Press Release:
    Research reveals new understanding, warning signs, and potential treatments for multiple sclerosis
     
  7. NewsBot

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    Press Release:
    FDA approves new MS treatment regimen developed at Wayne State University
    Higher dose, fewer injections for patients around the world

     
  8. NewsBot

    NewsBot The Admin that posts the news.

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    Press Release:
    Antibody May Be Detectable in Blood Years Before MS Symptoms Appear
     
  9. NewsBot

    NewsBot The Admin that posts the news.

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    Stem cell treatment halts MS progression in 91% of patients

    High-Dose Immunosuppressive Therapy and Autologous Hematopoietic Cell Transplantation for Relapsing-Remitting Multiple Sclerosis (HALT-MS)
    A 3-Year Interim Report

    Richard A. Nash et al
    JAMA Neurol. Published online December 29, 2014
     
  10. NewsBot

    NewsBot The Admin that posts the news.

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    Press Release:
    How multiple sclerosis can be triggered by brain cell death
    Nanoparticles stop the progressive disease and are being developed for humans
    Surprise finding: death of cells that make myelin can initiate MS
    Nanoparticles prevent progressive MS in animal model
    "Intervening early in disease will have greatest impact"
     
  11. NewsBot

    NewsBot The Admin that posts the news.

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    Press Release:
    Breakthrough may stop multiple sclerosis in its tracks
     
  12. NewsBot

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    Rehabilitation in Multiple Sclerosis: a Systematic Review of Systematic Reviews
    Fary Khan, MBBS, MD, FAFRM (RACP), Bhasker Amatya, MD, MPH
    Archives of Physical Medicine and Rehabilitation; in press
     
  13. NewsBot

    NewsBot The Admin that posts the news.

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    FDA News Release
    FDA approves Zinbryta to treat multiple sclerosis
    For Immediate Release
    May 27, 2016
     
  14. NewsBot

    NewsBot The Admin that posts the news.

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    Press Release:
    Multiple sclerosis: Newly discovered signal mechanism causes T cells to turn pathogenic
     
  15. NewsBot

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    PUBLIC RELEASE: 9-JAN-2017
    Breakthrough in MS treatment
    Drug shown to reduce new attacks/symptom progression in some patients

     
  16. NewsBot

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    PUBLIC RELEASE: 8-FEB-2017
    Study sheds light on the biology of progressive form of multiple sclerosis
    Suggests a new potential path for treatment
     
  17. NewsBot

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    The Effects of Tai Chi on Physical and Psychosocial Function among Persons with Multiple Sclerosis: A Systematic Review
    Emily Taylor, , Ruth E. Taylor-Piliae
    Complementary Therapies in Medicine 2 March 2017
     
  18. NewsBot

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    PUBLIC RELEASE: 20-JUL-2018
    A molecular key for delaying the progression of Multiple Sclerosis is found

    Multiple Sclerosis is an autoimmune disease that attacks and destroys a structure known as the "myelin sheath", whose integrity is indispensable for the brain and spinal cord to function properly.

    Current treatment of Multiple Sclerosis is based on modulating the activity of the immune system or preventing its cells from accessing the central nervous system and damaging it. These therapies are effective in the early phases of the disease, but they do not prevent its advance and the progressive functional deterioration.

    During the progressive phase of the disease it is the microglial cells in the brain that are the main cause of the chronic inflammation responsible for the neurological deterioration. These microglial cells are the brain's sentries and react when faced with any damage or infection in it. This reaction, which is in principle beneficial, becomes harmful when it is prolonged over time, leading to chronic inflammation, and aggravates the disease and encourages its progression.

    In the work just published it was possible to identify a receptor known as P2X4 present in the microglial cells that increases their anti-inflammatory potential in order to reduce the damage in Multiple Sclerosis and, above all, encourage the body's own repair responses.

    This experimental development was conducted using animal models of this disease, thanks to which it was possible to discover that the drugs that activate this receptor improve the symptoms during the chronic phase of the disease when furthering the repair of the nervous tissue.

    As Dr María Domercq of the UPV/EHU's Department of Neurosciences and who works at the ACHUCARRO centre for research in Leioa (Basque Country) pointed out, "We are witnessing a discovery that is opening up a new channel of pharmacological development for the treatment of the progressive phase of Multiple Sclerosis, and with it we want to open a new door on improving the life quality of people who suffer Multiple Sclerosis".

    This ambitious study was developed by an international research group coordinated from the Basque Autonomous Community, specifically from Leioa, with research personnel from the ACHUCARRO research centre, the UPV/EHU, ciberNed and CICbiomaGUNE in collaboration with the technical contribution of professionals from the University of Hamburg in Germany, and the Institut de Génomique Fonctionnelle in Montpellier, France.
     
  19. NewsBot

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    PUBLIC RELEASE: 22-JAN-2019
    Multiple sclerosis -- Helping cells to help themselves
    Researchers decipher one of the body's brain regeneration mechanisms


    Diseases such as multiple sclerosis are characterized by damage to the 'myelin sheath', a protective covering wrapped around nerve cells akin to insulation around an electrical wire. Researchers from Charité - Universitätsmedizin Berlin have discovered how the body initiates repair mechanisms which will limit the extent of any damage to this sheath. Their findings, which provide a basis for the development of new drugs to treat multiple sclerosis, have been published in the eminent journal Nature Communications*.

    Multiple sclerosis is the most common autoimmune disease of the central nervous system. Estimates suggest that more than 200,000 people are affected by the disease in Germany alone. People with multiple sclerosis experience vision and sensory problems, as well as impaired coordination or even paralysis. These symptoms are caused by the disruption of nerve impulses in either the brain or the spinal cord. This disruption occurs when the body's immune system attacks the myelin sheath, which is wrapped around the body's nerve fibers and provides electrical insulation. When the myelin sheath is no longer intact, communication between nerve cells is impaired. Researchers across the globe are searching for new ways to repair the myelin sheath and, in doing so, are looking to reduce neurological symptoms in people with multiple sclerosis. Researchers from Charité have now moved a decisive step closer to this goal.

    Charité's research team decided to take a closer look at the body's innate ability to heal itself, knowing that, under certain conditions, the central nervous system is capable of repairing damage to the myelin sheath. Specific molecular signals enable stem cells to differentiate into myelin repair cells (oligodendrocytes), which reside in a small stem-cell niche in the brain. Once they leave this niche, these repair cells migrate to where myelin damage has occurred in order to restore the affected nerve cells' electrical insulation. Until now, very little had been known about the molecular signals responsible for initiating this myelin regeneration mechanism. "We have found that the Chi3l3 protein plays a central role in the body's capacity to produce new myelin-forming oligodendrocytes," says the study's first author, Dr. Sarah-Christin Staroßom of Charité's Institute for Medical Immunology. A researcher at the NeuroCure Cluster of Excellence and the Experimental and Clinical Research Center (ECRC), Dr. Staroßom explains the protein's role as follows: "The Chi3l3 protein initiates the differentiation of neural stem cells into myelin repair cells, which restore the electrical insulation around damaged nerve cells."

    Using a mouse model, the research team were able to show that a reduction in Chi3l3 levels in the brain significantly impairs the body's capacity for oligodendrocyte production, while a Chi3l3 infusion leads to an increase in the production of myelin repair cells. The same reaction was observed during an in vitro experiment using human cells. "We hope to use this knowledge to develop a new generation of drugs that can be used in the treatment of multiple sclerosis," explains Dr. Staroßom. "As a next step, we will study in greater detail whether Chi3l3 or related proteins can be used to reduce the neurological symptoms of patients with multiple sclerosis."
     
  20. NewsBot

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    PUBLIC RELEASE: 24-JAN-2019
    Multiple sclerosis: Perilous ruptures

    The permanent neurological deficits of multiple sclerosis patients largely depend on the extent of degeneration of long nerve fibers. The latter is initiated by ruptures in the cell membrane and the resulting influx of calcium ions.

    In Germany alone, more than 200,000 patients suffer from multiple sclerosis (MS). MS is an autoimmune condition and one of the most common inflammatory diseases of the central nervous system. The degree of the patient´s disability, is critically dependent on the extent of nerve-fiber loss. This is because the autoimmune reaction characteristic of the condition attacks the long processes, called axons, which are responsible for the transmission of nerve impulses. Now a team led by Professor Martin Kerschensteiner, Director of the Institute of Clinical Neuroimmunology at Ludwig-Maximilians-Universitaet (LMU) in Munich, and Professor Thomas Misgeld of the Institute for Neuronal Cell Biology at the Technical University of Munich (TUM), working with an animal model of MS has identified a putative mechanism that can result in the degeneration of axons. They have shown that minuscule ruptures in the cell membrane allow calcium ions to percolate into the neuron, disrupting the ionic balance and ultimately killing the axon. The new findings appear in the journal Neuron.

    In previous studies, Kerschensteiner, Misgeld and colleagues had observed that axons in inflammatory lesions often were swollen and subsequently fragmented. "But in some cases, the swelling spontaneously regressed and these axons recovered," says Kerschensteiner. "So the process is in principle reversible, and could perhaps be therapeutically modulated if we had a better understanding of the underlying mechanisms." With the aid of in-vivo microscopy, the researchers have now shown in an animal model of MS that the fate of these axons depends on their calcium content. Axons with an abnormally high concentration of calcium are more likely to undergo swelling and subsequent degeneration and less likely to recover from this state than axons with normal levels of the ion. "Strikingly, these changes begin relatively early in the course of the axon damage process," says Misgeld. Indeed, in 10% of the axons examined, the calcium concentration was already increased prior to the onset of swelling. About half of the swollen axons were found to have high levels of intracellular calcium, and a correspondingly high risk of degeneration.

    The excess calcium is derived from the extracellular space and it enters the axon via nanoruptures in the cell membrane, as the team was able to demonstrate using a fluorescent dye coupled to a macromolecule. "The complex is too large to penetrate into an intact axon. Only if the membrane has been damaged can it be taken up into the axon and detected by its fluorescence. With the aid of in-vivo microscopy, we were also able to show that many of the axons that take up the dye also contain increased amounts of calcium," says Kerschensteiner. "The fact that, in the inflamed nervous system, tears in the cell membrane can contribute to the death of nerve fibers is a new discovery, which could in future be therapeutically relevant." adds Misgeld. It is already known from studies of spinal cord injury that nerve cells have the capacity to repair ruptures caused by mechanical forces. The researchers therefore hope that a better understanding of the origins and repair of damaged nerve-cell membranes will bring them closer to identifying new targets for therapeutic interventions.
     
  21. NewsBot

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    FDA News Release
    FDA approves new oral drug to treat multiple sclerosis
    March 26, 2019
    The U.S. Food and Drug Administration today approved Mayzent (siponimod) tablets to treat adults with relapsing forms of multiple sclerosis (MS), to include clinically isolated syndrome, relapsing-remitting disease, and active secondary progressive disease.

    “Multiple sclerosis can have a profound impact on a person’s life,” said Billy Dunn, M.D., director of the Division of Neurology Products in the FDA’s Center for Drug Evaluation and Research. “We are committed to continuing to work with companies that are developing additional treatment options for patients with multiple sclerosis.”

    MS is a chronic, inflammatory, autoimmune disease of the central nervous system that disrupts communications between the brain and other parts of the body. Most people experience their first symptoms of MS between the ages of 20 and 40. MS is among the most common causes of neurological disability in young adults and occurs more frequently in women than in men.

    For most people, MS starts with a relapsing-remitting course, in which episodes of worsening function (relapses) are followed by recovery periods (remissions). These remissions may not be complete and may leave patients with some degree of residual disability. Many, but not all, patients with MS experience some degree of persistent disability that gradually worsens over time. In some patients, disability may progress independent of relapses, a process termed secondary progressive multiple sclerosis (SPMS). In the first few years of this process, many patients continue to experience relapses, a phase of the disease described as active SPMS. Active SPMS is one of the relapsing forms of MS, and drugs approved for the treatment of relapsing forms of MS can be used to treat active SPMS. Later, many patients with SPMS stop experiencing new relapses, but disability continues to progress, a phase called non-active SPMS.

    The efficacy of Mayzent was shown in a clinical trial of 1,651 patients that compared Mayzent to placebo in patients with SPMS who had evidence of disability progression in the prior two years and no relapses in the three months prior to enrollment. The primary endpoint of the study was the time to three-month confirmed progression in disability. The fraction of patients with confirmed progression of disability was statistically significantly lower in the Mayzent group than in the placebo group. Mayzent also decreased the number of relapses experienced by these patients. In the subgroup of patients with non-active SPMS, the results were not statistically significant.

    Mayzent must be dispensed with a patient Medication Guide that describes important information about the drug’s uses and risks. Mayzent may increase the risk of infections, so patients should have a complete blood count taken before treatment is initiated. The drug may cause macular edema, so patients should contact their physician if they experience a change in vision. Mayzent may cause transient decreases in heart rate and may cause a decline in lung function. Liver enzymes should be checked before initiation of the drug and health care professionals should closely monitor patients with severe liver impairment. Health care professionals should monitor the patient’s blood pressure during treatment. Women of childbearing potential should use effective contraception during and for 10 days after stopping the drug due to the potential risk of fetal harm. Health care professionals should monitor patients for posterior reversible encephalopathy syndrome and monitor patients that had treatment with immunosuppressive/immune-modulating therapies because there may be unintended additive immunosuppression with Mayzent.

    The most common adverse reactions reported by patients receiving Mayzent in the clinical trials include headache, high blood pressure and liver function test increases.

    The FDA granted approval of Mayzent to Novartis.

    The FDA, an agency within the U.S. Department of Health and Human Services, protects the public health by assuring the safety, effectiveness, and security of human and veterinary drugs, vaccines and other biological products for human use, and medical devices. The agency also is responsible for the safety and security of our nation’s food supply, cosmetics, dietary supplements, products that give off electronic radiation, and for regulating tobacco products.
     
  22. NewsBot

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    NEWS RELEASE 20-APR-2020
    New therapeutic options for multiple sclerosis in sight

    Multiple sclerosis (MS) is known as "the disease with a thousand faces" because symptoms and progression can vary dramatically from patient to patient. But every MS patient has one thing in common: Cells of their body's own immune system migrate to the brain, where they destroy the myelin sheath - the protective outer layer of the nerve fibers. As a result, an electrical short circuit occurs, which prevents the nerve signals from being transmitted properly.

    Many MS medications impair immune memory

    Researchers don't yet know exactly which immune cells are involved in stripping away the myelin sheath. Autoreactive T and B cells, which wrongly identify the myelin sheath as a foreign body, travel to the brain and initiate the disease. "Up until now, MS drugs have essentially targeted these T and B cells, both of which are part of the acquired immune system," says Dr. Alexander Mildner, a scientist at the Max Delbrück Center for Molecular Medicine in the Helmholtz Association (MDC) and the senior author of the paper now published in Nature Immunology.

    Mildner is currently conducting externally funded research as a DFG Heisenberg fellow in Professor Achim Leutz's lab at the MDC, which focuses on cell differentiation and tumorigenesis. "But by attacking the acquired immune system, the MS drugs adversely affect the body's immune memory, thus making patients more susceptible to infections in the long run," the scientist says.

    MS symptoms improved in mice by reducing monocytes

    As a result, Mildner has been pursuing a different strategy for a couple of years now. He wants to find out what role immune cells - particularly those that are part of innate immunity - play in the development of MS and whether they represent a promising target structure for therapy of MS patients. "In an earlier study with a mouse model of MS, we were able to show that disease symptoms in the mice declined significantly within a few days after their monocytes were selectively destroyed by antibodies," the researcher reports. This result came as a big surprise to him and to many of his colleagues. "Apparently, it is not only T and B cells that are involved in causing tissue damage in MS," Mildner says.

    The monocytes he studied are a special type of white blood cells that shortly circulate in the blood before migrating into tissue. Once there, they transform themselves into effector cells (phagocytes) and destroy foreign tissue in the central nervous system (CNS) - or which, during MS, they wrongly identify as such. "This process," Mildner says, "leads to inflammation and tissue damage in the brain."

    The team discovered unknown types of monocytes

    In the current study published in Nature Immunology, which he conducted in collaboration with an Israeli team led by Professor Ido Amit from the Department of Immunology at the Weizmann Institute of Science, Mildner and his team also focused on monocytes. "During the last recent years we realized that several types of these immune cells exits, which might carry out different functions," the researcher says. "We therefore wanted to examine in our mouse model of MS the monocytes in greater detail using single-cell sequencing and to find out, which monocyte subsets are present in the brain in MS and are responsible for tissue damage."

    He and his colleagues identified six different monocyte subtypes, four of which were previously unknown. As in his earlier study, Mildner injected the mice with antibodies against a specific monocyte surface protein. As expected, the cells died and the MS symptoms in the mice decreased within a short period of time. "But what surprised us was that the antibodies did not destroy all monocyte subsets in the brain that have this surface protein," Mildner says.

    Not all monocytes destroy the protective myelin sheath

    "Only a certain type of monocyte, the Cxcl10+ cells, was destroyed by the antibody treatment," Mildner says. "These are apparently the cells that are primarily responsible for causing MS tissue damage in the brain." With the help of single-cell sequencing, he and his team also discovered that this cell type differs from other monocytes in two essential ways: First, Cxcl10+ cells have a particularly large number of receptors for a signal protein secreted by T cells that induces tissue damaging properties in monocytes. Second, these cells produce large amounts of interleukin-1-beta, a substance that opens the blood-brain barrier, enabling immune cells to more easily pass from the blood to the brain and exacerbate the symptoms. "Our research suggests that T cells, as disease initiators, travel to the CNS in order to lure there the monocytes that are responsible for the primary tissue damage," Mildner explains.

    The other monocyte subsets that were identified, he speculates, are perhaps even involved in repair processes in which the body tries to rebuild the damaged myelin. In light of the study's findings, he thinks it is also possible that the T and B cells are not even directly involved in stripping away the myelin sheath, but only indirectly in that they prompt the Cxcl10+ monocytes to attack the protective layer of the axons.

    Many side effects may be preventable

    "If that is the case, in the future most forms of MS could be treated by specifically deactivating the Cxcl10+ monocytes instead of targeting the T or B cells of the immune system," Mildner says. "This would protect the body's immune memory and prevent many side effects of current MS therapies." The researcher and his team next plan to investigate whether the Cxcl10+ monocytes are also present outside the CNS. "If they exist in the body's periphery, for example, in the lymph nodes," he says, "there they would be easier to target with therapeutics than in the brain."
     
  23. NewsBot

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    NEWS RELEASE 22-OCT-2020
    Multiple sclerosis as the flip side of immune fitness

    About half of the people with multiple sclerosis have the HLA-DR15 gene variant. A study led by the University of Zurich has now shown how this genetic predisposition contributes to the development of the autoimmune disease multiple sclerosis in combination with environmental factors. The decisive factor is the shaping of a repertoire of immune cells which - although they are effective in fighting off pathogens such as Epstein-Barr virus - also attack brain tissue.

    Multiple sclerosis is an autoimmune disease that damages the brain and the spinal cord and often severely limits a person's quality of life. It affects about 2.5 million people worldwide, most of them young adults. The cause of the disease is a complex interaction between genetic factors and environmental influences such as smoking or infections.

    Genetic variation and viruses as risk factors

    For almost 50 years now, it has been known that a gene variant called HLA-DR15 is strongly associated with multiple sclerosis (MS). This gene variant is responsible for up to 60 percent of genetic risk. If carriers of this common gene (about a quarter of the healthy population is HLA-DR15 positive) are also infected with the Epstein-Barr virus and have a symptomatic course of infection called Pfeiffer's disease (also known as glandular fever or infectious mononucleosis), the risk of MS increases 15-fold.

    UZH Professor Roland Martin, Head of the Department of Neuroimmunology and MS Research at the University Hospital Zurich, says: "There are therefore clear indications that the interaction between HLA-DR15 and infectious agents such as Epstein-Barr virus is significant for the development of the disease, even though the exact mechanisms behind this have not been understood until now."

    An interdisciplinary, international study led by Martin has now shown that the immune cells of people with HLA-DR15 recognize certain microbes - such as the Epstein-Barr virus - very effectively, but that this "fitness" can also lead to an undesired immune reaction against the person's own brain tissue.

    Individual training for immune cells

    The gene products of HLA-DR15 control how the adaptive immune system shapes an immune repertoire that allows the body to recognize and fight pathogens. One of the locations of HLA-DR15 molecules is on the surface of white blood cells. There, they present protein fragments from bacteria, viruses and body cells to the T lymphocytes of the immune system.

    The T lymphocytes - which later control the immune response - learn to distinguish between foreign proteins and the body's own tissue. This individual training of immune cells takes place first in the thymus and then in the blood. Since there are many more possible pathogens than T lymphocytes, each T lymphocyte must be able to respond to many different antigens and probably also many different pathogens.

    Identifying the fragments presented

    The researchers first investigated which fragments HLA-DR15 captured and presented to the immune cells. To do this, they used two novel antibodies that recognize the two variants of HLA-DR15 that occur in MS patients with a very high level of specificity. They found that the HLA-DR15 molecules in the thymus mainly present fragments of themselves. This is new information that was not previously known.

    The T lymphocytes that have been trained in this way then migrate into the blood. There, they also learn to recognize fragments of the Epstein-Barr virus if the carrier of the genetic variant becomes infected with it. The fragments from the virus have a much stronger activating effect than the HLA-DR15 fragments.

    As a result, the T lymphocytes not only keep virus-infected cells in check, but can also migrate to the brain and react with the body's own proteins that trigger an autoimmune reaction in the case of MS. Nearly 100 percent of people with MS are infected with the Epstein-Barr virus. It is the greatest environmental risk factor for MS. The researchers also often found a reaction to fragments of the intestinal bacterium Akkermansia muciniphila, which occurs in abnormally high numbers in MS patients.

    Good immune defenses come with a risk of MS

    Summarizing, Martin states that "The most important genetic risk factor for MS therefore shapes a repertoire of T lymphocytes that responds very well to certain infectious agents such as Epstein-Barr virus and intestinal bacteria." However, as the experiments have shown, this group of T lymphocytes also reacts to proteins found in the brain by way of a kind of cross-reactivity. "The disadvantage of this fitness is therefore that those affected also become susceptible to an immune response against their own brain tissue, which can lead to multiple sclerosis."

    Therefore, these results have for the first time illustrated how the combination of genetic predisposition and certain environmental factors can trigger an autoimmune disease. "Our work has shed light on mechanisms that are likely to play a role in a number of other autoimmune diseases," says Martin. "In addition to improving our understanding of underlying causes of the disease, this could also lead to the development of new treatments".
     
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