Inhibition of Cytokine-Induced MHC Class II but Not Class I Molecule Expression on Mouse Islet Cells by Niacinamide and 3-Aminobenzamide
- Division of Endocrinology and Metabolism, Department of Medicine, Kurume University School of Medicine Asahimachi, Kurume, Fukuoka, Japan
- Address correspondence and reprint requests to Dr. K. Yamada, Division of Endocrinology and Metabolism, Department of Medicine, Kurume University School of Medicine, Asahimachi, Kurume, Fukuoka 830, Japan.
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.
- Received September 29, 1989.
- Revision received April 30, 1990.
- Accepted April 30, 1990.
- Copyright © 1990 by the American Diabetes Association