Cytoldnes, particularly interferons, may participate in the development of type I diabetes. This involvement could be from direct cytotoxic actions of the interferons on the pancreatic (β-cells or from an indirect influence on the number, activity, or type of inflammatory cells that invade the islets in type I diabetes. To examine directly the role of interferon (IFN)-γ in a mouse model of type I diabetes, we have introduced an inactivating mutation in the IFN-γ gene (ifg) into NOD mice. The genetic absence of IFN-γ does not prevent either insulitis or diabetes in the NOD mice, but it does increase the time to onset. Although it might have been predicted that the absence of IFN-γ in these mice would lead to an increase in expression of Th2 T-helper cell-related cytoldnes, we found instead a profound decrease in the expression of two of the characteristic Th2 cytoldnes, interleukin (IL)-4 and EL-1O. We also demonstrate that the splenocytes taken from IFN-γ–deficient diabetic mice are fully capable of transferring diabetes to naive recipients.

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