Predicting Type I Diabetes

Abstract

Accumulating data has led to the general hypothesis that Type I diabetes of the NOD mouse (non-obesediabetic), BB rat (BioBreeding rat) and man results from chronic autoimmune beta cell destruction (1). The information supporting this hypothesis is briefly summarized in Table 1 and includes the detection of anti-islet autoantibodies prior to diabetes; presence of T lymphocytic islet infiltrates; the observation that in all three species a gene within the major histocompatibility complex is essential for the development of diabetes; the ability of multiple forms of immunotherapy to prevent diabetes in animal models and randomized placebo controlled trials of cyclosporine A in man (2) (the nephrotoxicity of cyclosporine is a major concern which prevents widespread clinical application of cyclosporine therapy of Type I diabetes); the recurrence of disease in transplanted islets which have been treated to prevent tissue rejection in animal models and similar recurrence in identical twin pancreatic transplants; and in the finding both animal models that T lymphocytes can transfer diabetes.