ABSTRACT
This chapter deals with the trials attempted to intervene in the development of diabetes or insulitis in the nonobese diabetic (NOD) mouse. Accumulating evidence strongly suggests that insulin-dependent or Type I diabetes mellitus is of an autoimmune origin. Since the diabetic syndrome of the NOD mouse is clearly immune-mediated, it has been hoped that this animal would provide a useful model for evaluation of immunosuppressive therapy in human Type I diabetes. Since the lymphocytes infiltrating the islets of NOD mice are mainly T cells, it is reasonable to speculate that the thymus might have some role in the pathogenesis of insulitis in these mice. Cyclosporine, a potent immunosuppressive agent, seems to derive its action from inhibition of the release of interleukin-1 and -2, both of which are involved in the generation of helper T cells. The original assumption was that the agent might accelerate the development of diabetes in NOD mice by inducing obesity.
