PITTSBURGH, Jan. 8 University of Pittsburgh investigators have successfully prevented the onset of type 1 diabetes in mice prone to developing the disease using an antibody against a receptor on the surface of immune T-cells. According to the investigators, these findings, which are being published in the January issue of the journal Diabetes, have significant implications for the prevention of type 1 diabetes.

More than 700,000 Americans have type 1 diabetes, an autoimmune disorder in which the body errantly attacks the insulin-producing cells of the pancreas, causing chronically elevated levels of sugar in the blood, leading to blindness, kidney failure, heart disease and nerve damage. Previously known as juvenile diabetes, type 1 diabetes is usually diagnosed at a very early age, but in some cases it can be diagnosed in adulthood.

In this study, the Pitt researchers treated non-obese diabetic (NOD) mice with an antibody -- a type of protein produced by the immune system that recognizes and helps fight infections and other foreign substances in the body -- directed against a receptor known as CD137 on the surface of a type of immune cell called T-cells. Treating NOD mice with the anti-CD137 antibodies significantly suppressed the development of diabetes, whereas most of the control mice developed diabetes by the time they were six months old.

Interestingly, the antibody therapy did not appear to cure the NOD mice because the researchers were still able to see lymphocytes in their pancreatic islets, a tell-tale sign of pancreatic inflammation and autoimmunity. In addition, when the researchers isolated cells from the spleens of the antibody-treated mice and injected these cells into immune-deficient NOD mice, seven of the nine recipient mice developed type 1 diabetes, indicating that the donor mice still harbored pathogenic T-cells. On the other hand, when the researchers transferred a certain subset of T-cells from anti-CD137-trea
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Contact: Jim Swyers
swyersjp@upmc.edu
412-647-3555
University of Pittsburgh Medical Center
8-Jan-2007