IL-10 exterts profound immunostimulatory and immunoinhibitory effects. To explore the role of IL-10 in autoimmune diabetes of nonobese diabetic (NOD) mice, we generated IL-10-deficient NOD mice. In contrast to our previous results with neutralizing anti-bodies to IL-10, IL-10-deficient NOD mice developed insulitis and their splenocytes readily responded to islet antigen glutamic acid decarboxylase 65. IL-10-deficient NOD mice did not develop accelerated spontaneous diabetes. On the other hand, IL-10-deficient NOD mice developed accelerated disease following cyclophosphamide (CYP) injection. These findings demonstrate that IL-10 is dispensable for autoimmune diabetes. IL-10's absence fails to accelerate endogenous diabetes but potentiates CYP-induced diabetes. (C) 2000 Academic Press.
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