Normal mouse islet cells express low levels of MHC class I molecules and undetectable or extremely low levels of MHC class II molecules. Class I expression was dose-dependently augmented by incubation with interferon-γ (IFN-γ) or tumor necrosis factor (TNF). Although neither IFN-γ nor TNF alone induce class II molecules on islet cells, synergistic interaction of IFN-γ (200 U/ml) and TNF (200 U/ml) may induce class II expression on ∼50% of islet cells. Niacinamide and 3-aminobenzamide, both inhibitors of ADP ribosylation and scavengers of free radicals, attenuated the class II expression induced by IFN-μ and TNF. Twenty millimolar niacinamide and 10 mM 3-aminobenzamide reduced the rates of class II antigenpositive cells to mean ± SD 3.6 ± 0.3 and 6.1 ± 1.9%, respectively. The agents did not affect the cytokineinduced augmentation of class I antigens. The inhibition of class II molecule expression may at least partly account for the preventive effect of niacinamide on autoimmune-associated α-cell damage in NOD mice.

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