{"id":299904,"date":"2022-02-10T16:10:51","date_gmt":"2022-02-10T21:10:51","guid":{"rendered":"https:\/\/yfile.news.yorku.ca\/?p=299904"},"modified":"2025-04-02T13:20:34","modified_gmt":"2025-04-02T17:20:34","slug":"working-toward-treatment-for-rheumatoid-arthritis","status":"publish","type":"post","link":"https:\/\/www.yorku.ca\/yfile\/2022\/02\/10\/working-toward-treatment-for-rheumatoid-arthritis\/","title":{"rendered":"Working toward treatment for rheumatoid arthritis"},"content":{"rendered":"\n
By Elaine Smith<\/em><\/strong><\/p>\n\n\n\n Research by Ali Abdul-Sater<\/strong>, a York Research Chair in the Regulatory Mechanisms of Inflammation, and an assistant professor in the School of Kinesiology & Health Science, Faculty of Health, has determined that a specific protein, TRAF1, holds the key to controlling inflammation in rheumatoid arthritis and a specific mutation to the protein can reduce the amount of inflammation the joints experience. With funding from the Canadian Institutes for Health Research, the Arthritis Foundation and ¿ì²¥ÊÓÆµ, Abdul-Sater and his research team are currently testing their findings in mice and hope the results will eventually translate to humans.<\/p>\n\n\n\n \u201cWe are planning to use TRAF1 to develop new therapy for rheumatoid arthritis and other inflammatory diseases,\u201d Abdul-Sater says. \u201cI wouldn\u2019t wish rheumatoid arthritis on anyone; it is one of the most painful chronic diseases and it becomes progressively worse. For some sufferers, it can take hours just to get their joints moving each morning.\u201d<\/p>\n\n\n\n Abdul-Sater calls TRAF1 \u201cthe Swiss army knife of proteins\u201d because it serves different functions in different immune cells. He discovered that TRAF1 can control or limit inflammation by preventing certain immune cells (macrophages) from producing too many cytokines that destroy the joints; on the other hand, previous research indicated that TRAF1 is also known to activate other immune cells (lymphocytes) and enhance their ability to produce antibodies or cytokines that damage the joints. The key is to find a way to stop TRAF1 from activating lymphocytes while preserving its ability to limit inflammation and cytokine production.<\/p>\n\n\n\n It turns out that TRAF1 is a scaffold, or a platform, from which these signals are sent out. Abdul-Sater found that each of its functions used a different type of scaffold, so he was able to disrupt one function while leaving the other intact. In fact, he discovered a specific genetic mutation that does just that: it prevents immune cells from overproducing antibodies while suppressing its joint-destroying cytokine production, thus reducing inflammation and keeping the joint intact.<\/p>\n\n\n\n