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Researchers Test a New Approach to Reduce Immune Reactions in Type 1 Diabetes

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The most common form of type 1 diabetes is caused by an autoimmune reaction (the body attacks its own healthy cells) that destroys insulin-producing β cells. Because most newly diagnosed patients with diabetes still produce significant amounts of insulin, preserving remaining β-cell function is desirable to reduce short- and long-term complications of the disease. Because T cells play a central role in the type 1 diabetes autoimmune reaction, researchers investigated whether a drug that works to partially block T-cell function could benefit patients with early-stage type 1 diabetes.

In a randomized clinical trial, supported in part by the Pediatric Growth and Nutrition Branch, involving 112 patients, 77 were assigned to receive treatment with abatacept, a drug used to treat rheumatoid arthritis (also an autoimmune disease) by blocking the activity of T cells. The remaining patients received placebo treatments. The results showed that abatacept had an early beneficial effect in slowing the reduction in β-cell function. However, over a 24-month period, the drop in β-cell function in the abatacept group paralleled that in the placebo group. Moreover, patients receiving abatacept had similar insulin doses at the end of the study, although the abatacept patients did produce slightly more insulin from their own bodies. 

Although these results indicated that abatacept is not appropriate for clinical use at this time, scientists plan further studies to see if abatacept may be useful as part of a combination therapy in recent-onset type 1 diabetes (PMID: 21719096).

Last Reviewed: 05/01/2014
Vision National Institutes of Health Home BOND National Institues of Health Home Home Storz Lab: Section on Environmental Gene Regulation Home Machner Lab: Unit on Microbial Pathogenesis Home Division of Intramural Population Health Research Home Bonifacino Lab: Section on Intracellular Protein Trafficking Home Lilly Lab: Section on Gamete Development Home Lippincott-Schwartz Lab: Section on Organelle Biology