IL-1 induces intracisternal type A virus and retrovirus type C in pancreatic beta-cells of NOD mice.

Recent observations have suggested a role for interleukin 1 (IL-1), a macrophage-derived cytokine, in the autoimmune beta-cell destruction, that is associated with type 1 diabetes. In this study, we investigated the effects of human recombinant IL-1 beta on pancreatic beta-cells from NOD and NON mice (diabetes-resistant NOD-related strain), focussing upon the appearance of intracisternal type A virus (IAP) and retrovirus type C. NOD mice pancreatic islets were incubated with or without IL-1 (0.1, 1, 10, 100 U/ml) for 10 days. Thereafter, the islets were examined using an electron microscope. When the islets of NOD mice were incubated with the IL-1 (10, 100 U/ml) under condition of high glucose, IAP and endogenous retrovirus type C frequently appeared in the beta-cells. Retrovirus type C was present as a cluster. In contrast, IAP and retrovirus type C were rarely found in beta-cells from the control group. When the islets of NON mice were incubated with or without IL-1 (10 U/ml) in the presence of high glucose, IAP was rarely found in beta-cells and retrovirus type C was undetectable in beta-cells. This study indicated that IL-1 is an important effector that leads to insulitis or aggravates insulitis in NOD mice.