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The main reason that MS tends to run in familiesTwo new animal models with relevance for human MS: mice transgenicfor an anti-MOG T-cell receptor or for MS associated HLA DQ6 http://www.mssociety.ca/en/research/projects/immunology.htm#elliott$51,880 (April 1/00 - March 31/01)The main reason that MS tends to run in families is that certaingenes contribute to developing the disease, and of course we inherit our genes from our parents. So far, the only group of genes that has been clearly linked to an increased risk of MS is the HLA (HumanLymphocyte Antigens) class II genes. These genes are at the crux of the immune system's ability to function as they dictate what spectrum of things the immune system cells can respond to.The focus of this project is to study why one particular HLA gene, called HLA-DQ, might be associated with MS. There are many different types of DQ genes in people, but it turns out people with DQ6 are at increased risk for MS. To help him study this, Dr. Elliot has developeda DQ transgenic mouse that contains virtually identical human DQ6 genes as those found in people who are likely to get MS. He anticipates that most of the immune responses in the DQ6 transgenic mouse will likely mimic those found in humans. Dr. Elliot is also developing anothertransgenic mouse model of MS, called anti-MOG TCR, to help him study the immune system attack on myelin.Because it is impossible to study many aspects of MS in humans, it is necessary to develop different animal models of MS. Both the HLA-DQ6 and anti-MOG TCR transgenic mouse models will be extremely useful for testing new therapies against MS.Y. scientists contribute to immune discoveryBy Lois M. Deseret Morning NewsFriday, November 12, 2004http://deseretnews.com/dn/view/0,1249,595104911,00.html Brigham Young University scientists are on an international team that has figured out how the body regulates its immune response. Thatmay unlock doors to prevent or treat autoimmune illnesses like lupus, multiple sclerosis and rheumatoid arthritis. And it could helpexplain how the body rallies to fight invaders like viruses, bacteria andeven cancer. The discovery was being published today in Science Express, the online version of the journal Science, and will later appear in the print edition of the journal. Their research found the "key"that controls natural killer T cells, "the regulatory cells in the immune system that help control the type of immune responses it cangenerate" such as inflammation, said B. Savage, professor of chemistry and biochemistry at BYU. That response is also responsible for multiple sclerosis, rheumatoid arthritis, lupus and other autoimmune-generated illnesses. The natural killer T cells recently debuted on the world stage as key immune system regulators. What this research adds is evidence of the identity of the specific key antigen that signals the immuneresponse. And this antigen is different from most known antigens, which are typically small pieces of protein. This one is a glycolipid,comprised of sugar and fatty molecule. While scientists knew an antigen turned on the natural killer T cells because they could see what it did, Savage and his colleagues are the first to identify it. That will allow them to study where the key is made, what regulates it and how the responses are controlled, hesaid. They hope to manipulate the natural killer T cells to treat disease. They also plan to create an artificial form of the antigen to see if they can slow down or speed up immune system response. The same antigen that "selects" natural killer T cells for duty also has to be present for the natural killer T cells to form, Savage said. Without it, they don't survive.In autoimmune diseases, the body attacks itself, using inflammation. It can result from lack of natural killer T cells, which are supposed to moderate immune response to protect without damaging the body. Savage believes people with autoimmune diseases may not have enoughof the antigen. By knowing what the natural antigen looks like, "we can in the future design synthetic keys to switch" the response on and off, he said. "We've already done this to some extent." Last year, Savage and his colleagues published a paper in Science that hinted at what the key antigen might be. Identifying it, he said, would be "the Holy Grail for us." Savage and two graduate students, Ning Yin and Ying Gao, are organic chemists who made the artificial antigens for the research. He said that many researchers all over the world have sought this antigen,but teaming organic chemists with immunologists made the discovery possible.He's hopeful that resulting treatments won't be too far down theroad. "A lot of the work's already been done. Things are moving forward pretty rapidly. In terms of stimulating inflammatory response, there are already things in clinical trials" against diseases like hepatitis. "For treatment of autoimmunity, animal models are very encouraging."Much natural killer T cell research is occurring worldwide becausethe cells play such a strong role in immune system response. "They are an attractive means of influencing immune responses," Savage said. "They work at the headwaters all the way upstream. Instead of treating symptoms, they treat effects." Lead authors are Dapeng Zhou and Albert Bendelac at the University of Chicago. Co-authors are the BYU team and researchers from the Scripps Research Institute, National Institutes of Health, GoteborgUniversity in Sweden, the Chinese Academy of Sciences and the University of New Hampshire.http://deseretnews.com/dn/view/0,1249,595104911,00.html E-mail: lois@...

Viral infections can accelerate autoimmune disorders posted by art on 08:08 AM November 16th, 2004http://www.bostoncure.org:8080/article.pl?sid=04/11/16/1311211 & mode=nocomment Research hollie writes "It is generally accepted in the scientific community that a genetic predisposition helps determine who will develop MS, but that other factors must be involved as well. Infections from viruses, bacteria, etc. are one possible type of trigger and indeed several different pathogens have been and/or currently are under scrutiny for a link with MS. While this work goes on, a team of scientists from the La Jolla Institute for Allergy and Immunology is approaching the issue from the other side, trying to find out exactly how an infection might hasten development of a disease in someone who is genetically susceptible to it. Theyexplored this question in a mouse model of type 1 diabetes, a strain of mice genetically engineered to express a viral antigen (from the LCMV virus) in its pancreas. Infection of this mouse with the LCMV virus itself results in an autoimmune attack of the pancreas thateventually (after several weeks) leads to signs of diabetes. This occurs through a process called molecular mimicry, where an immune response to a pathogen-expressed antigen also winds up targeting a similar self-antigen. In the case of this strain of mice, the autoimmune process continues even after the virus has been eliminated from the body." continued... "In their experiment, after first infecting the mice with LCMV and setting the autoimmune reaction in motion, the scientists infected them with a second virus, PV, which has an antigen in common withLCMV but cannot cause diabetes on its own. They found that the PVinfection dramatically sped up the development of diabetes, most likely through the activation and expansion of previously established cross-reactive T cells. Therefore while LCMV can cause diabetes on its own, LCMV followed by PV makes this happen faster. In this paper the authors also refer to similar work done using the Theiler's virus model ofMS, to be described in a later publication, which will further expand on this type of mechanism.What does this have to do with MS? It must be acknowledged that these types of models are highly experimental, using genetically engineered animals and intentionally administered infections which is not how MS or other human diseases develop. Furthermore, it isn't yet proventhat MS is actually an autoimmune disease (a disease that is driven by the immune system targeting a self-antigen). However, if further research into the medical histories of people with MS reveal higherfrequencies of certain patterns of infections prior to development of MS, the types of findings revealed in this paper may help us betterunderstand the role that those infections may have played." http://www.bostoncure.org:8080/article.pl?sid=04/11/16/1311211 & mode=nocomment

Viruses may trigger autoimmune diseasesUnited Press InternationalTuesday, November 2, 2004http://www.nlm.nih.gov/medlineplus/news/fullstory_20995.html SAN DIEGO, Nov 02, 2004 (United Press International via COMTEX) – Viruses alone may not cause autoimmune diseases like rheumatoid arthritis but can accelerate them in genetically predisposed people, U.S. researchers report.Scientists found mice predisposed to diabetes were more likely to develop the disease if exposed to a virus. Diabetes, lupus, multiple sclerosis and rheumatoid arthritis are examples of diseases where the body's immune system mistakenly attacks healthy tissue. Researchers believe the body may act correctly to repel an invading virus butthen extend its attack to molecules similar to those in the virus. Normal cells containing those molecules may then be damaged.The finding could help in the future development of therapies for the treatment or prevention of diabetes and other autoimmune illnesses."By building on this research, we may one day be able to advisepeople genetically predisposed to multiple sclerosis, for instance, to avoid certain viruses or bacteria or to be vaccinated against them in order to prevent actual development of autoimmune disease," wrote Kronenberg, president and scientific director of San Diego's La Jolla Institute for Allergy & Immunology, where the research took place.A report on the study appeared in this week's Journal of Clinical Investigation.-----Forwarded Message-----From: ineSG@...Sent: Nov 16, 2004 2:15 PMmsers_online Cc: PAULINESG@...Subject: [MSers_Online] Aricept May Help Memory in Multiple SclerosisAricept May Help Memory in Multiple Sclerosis By _Miranda Hitti_ (http://aolsvc.health.webmd.aol.com/content/Biography/8/101415.htm) WebMD Medical News Reviewed By _Brunilda Nazario, MD_ (http://aolsvc.health.webmd.aol.com/content/Biography/8/102316.htm) on Monday, November 08, 2004 Nov. 8, 2004 -- Aricept, a drug used in treating Alzheimer's disease, might improve memory and mental function in some people with multiple sclerosis (MS), according to a new study. The report, published in the Nov. 9 issue of the journal Neurology, focused on 69 patients with multiple sclerosis who suffered from mild declines in mental function. Multiple sclerosis is a chronic neurological disease of the brain, spinal cord, and optic nerves. Roughly half of all multiple sclerosis patients experience problems with memory and thinking, making problems with mental skills a leading cause of disability from the disease, which currently has no cure. Multiple sclerosis can also impair muscle control, strength, vision, balance, and sensation. Aricept is used to treat many of the symptoms of Alzheimer's disease, such as memory loss, confusion, and problems with thinking and reasoning. Aricept is made by Pfizer, a WebMD sponsor. At the start of the new study researchers from the neurology department of the State University of New York at Stony Brook asked participants with multiple sclerosis-associated memory and mental impairment to perform memory and mental skills tests. Next, they divided the participants into two groups. One group took Aricept for 24 weeks, starting with 5 milligrams per day and increasing to 10 daily milligrams in the study's fourth week. The other group took a placebo for 24 weeks. At 24 weeks, participants were retested. Aricept patients had greater improvements in memory testing than the placebo group. Memory test scores for the Aricept group improved almost 14% from their initial scores. The placebo group improved less than 3% on their memory test scores. In addition, 66% of the Aricept group reportedly said their memory had gotten better, compared with only 32% of the placebo group. No serious side effects were seen from Aricept, except for unusual or abnormal dreams, which were reported by 34% of the Aricept group and 9% of the placebo group. Larger Aricept Trials Needed The results are promising but require further study, say the researchers, who included Krupp, MD. "Any treatment that would enhance the ability of persons with MS to meet the cognitive challenges of their daily lives would be very helpful," write Krupp and colleagues, calling for bigger studies. "Multiple sclerosis patients are typically prescribed numerous medications to treat their disorder, so that before any new symptomatic treatment is added, its efficacy should be well substantiated," they write. In a Neurology editorial, P. Murali Doraiswamy, MD, of Duke University Medical Center and Rao, PhD, of the Medical College of Wisconsin, agree. Praising Krupp's study as "a major advance," they suggest studying topics including length of treatment, long-term risks, and withdrawal effects in future research. ____________________________________ SOURCES: Krupp, L. Neurology, Nov. 9, 2004; vol 63: pp 1579-1585. Doraiswamy, P., Neurology, November 2004; vol 63: pp 1552-1553. WebMD Medical News: "Keeping Life Normal With Alzheimer's." News release, American Academy of Neurology.