Abstract
Abstract The Idd3 genetic interval confers protection against multiple autoimmune diseases, including type 1 diabetes and experimental autoimmune encephalomyelitis (EAE). However, the cellular and molecular mechanisms by which the Idd3 locus mediates suppression of autoimmunity have not been analyzed. The favored candidate gene in this interval is Il2, which has been shown to be polymorphic between susceptible and resistant strains of mice. IL-2 regulates the growth/death of effector T cells as well as the generation/maintenance of regulatory T cells (Tregs). We have examined both Tregs and effector T cells in NOD and NOD.Idd3 congenic mice and find that NOD.Idd3 Tregs are more suppressive and NOD.Idd3 effector T cells produce more IL-10 when compared to NOD-derived T cells. Interestingly, we find that both these effects are driven by NOD.Idd3-derived antigen presenting cells, suggesting that the protective effect of Idd3 is due to alterations in the APC compartment and not T cells themselves.
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