New research published in Diabetes explains dysfunctional immune response that leads to type 1 diabetes, and finds a protein that delays disease onset. Experimental mice lacking the protein develop diabetes faster. The research from Case Western Reserve University School of Medicine could help understand the development of type 1 diabetes. Type 1 diabetes, an autoimmune disease, makes up 5 percent of all cases of diabetes and usually affects children and young adults. It happens when T cells, white blood cells that normally protect the body from illnesses, mistakenly destroys the insulin-producing beta cells in the pancreas. The pancreas then produces no or little insulin, a hormone that helps the cells use the sugar in the blood. This finally leads to high blood sugar and causes various symptoms. Previously, scientists have reported that inhibiting the c-Rel protein might protect against arthritis and other autoimmune disorders. However, the new study demonstrates that this could accelerate the development of certain illnesses like type 1 diabetes. The c-Rel is a member of the nuclear factor κB (NF-κB) transcription factor family, and it plays a major role in T cell function. To study the role of c-Rel in diabetes, the research team used genetically modified diabetic mice without c-Rel. After examining the numbers of T cells in these mice, the team identified a remarkable decrease in T regulatory cells, which is a subpopulation of T cells that suppress autoimmunity. Next, the team looked at T cells in the mice's pancreases, and discovered that T cells that induce immune responses displayed increased proliferation. Furthermore, c-Rel deficient mice became diabetic sooner than control mice. In addition, CusAb offers Recombinant RHO and c-Rel proteins and Biotin conjugated antibody.
