Researchers at the University of Utah School of Medicine have identified a potential new therapeutic target for the treatment of patients with type 1 diabetes. The study, which was published December 9, 2020 in the Journal of Experimental Medicine (JEM), reveals that inhibiting a protein called OCA-B protects mice from type 1 diabetes by limiting the activity of immune cells that would otherwise destroy the pancreas' insulin-producing β cells (https://rupress.org/jem/article/218/3/e20200533/211581/Targeting-transcriptional-coregulator-OCA-B). The open-access article is titled “Targeting Transcriptional Coregulator OCA-B/Pou2af1 Blocks Activated Autoreactive T Cells in the Pancreas and Type 1 Diabetes.” Type 1 diabetes is an autoimmune disease in which the body's immune system mistakenly attacks pancreatic β cells, cutting off the production of insulin. Patients require life-long insulin therapy to maintain appropriate blood glucose levels. At present, there are no treatments that can prevent the immune system from targeting β cells while preserving its ability to fight infection. White blood cells called T cells can recognize specific molecules produced by invading bacteria and viruses. When T cells encounter these molecules, known as antigens, they turn on hundreds of genes that allow them to fight the infection. A protein called OCA-B binds to many of these genes and helps ensure that they can easily be reactivated if the T cells reencounter the same antigens at a later date. In many autoimmune diseases, T cells mistakenly recognize and respond to antigens produced by normal, healthy cells.
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