Genetic flaw marks MS drug failure

Anti-TNF drugs have helped thousands of patients with autoimmune diseases like rheumatoid arthritis but actually make multiple sclerosis (MS) worse, but no one really knew why. At last, U.K. researchers have found a clue in a genetic marker that could explain why--and could also open up a route to new treatments or a way to select the patients who are most likely to respond and least likely to suffer from side effects. The team at Oxford University found that a genetic variant in the TNFRSF1A gene produced a short version of a protein that binds TNF (tumor necrosis factor). The short version mops up TNF outside cells, resulting in the same kind of effect as anti-TNF drugs. As the short version of the protein is linked with the risk of developing MS, this could explain why the anti-TNF drugs also make MS worse. Professor Lars Fugger of the Nuffield Department of Clinical Neurosciences at Oxford University says: "Whilst the TNFRSF1A gene variant is linked to a modest risk of developing MS, the drug that mimics the effect of the variant has a considerably greater impact. The effects of genetic variants influencing disease risk or resistance can be amplified by drugs." Press release | Abstract | Article

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