Abstract

The mechanism(s) leading to β cell dysfunction in type I diabetes has not been defined. We have investigated whether islet expression of IFNα could be a cause of the lesions that are hallmarks of type I diabetes. Streptozotocin induces the expression of interferon-α by pancreatic islets priorto the diabetes induced by streptozotocin. Increased IFNα, induced by poly I/C or expressed from a transgene will exacerbate the diabetogenic effects of streptozotocin. In another rodent model of type I diabetes (the BB rat), islet expression of IFNα precedes lymphocytic infiltration and diabetes. As in the streptozotocin model, in the BB rats poly I/C will induce islet expression of IFNα and accelerate the onset of diabetes. These results are consistent with the hypothesis that islet expression of IFNα participates in causing type I diabetes.

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call