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Interferon-γ Limits Diabetogenic CD8+ T-Cell Effector Responses in Type 1 Diabetes.


ABSTRACT: Type 1 diabetes development in the NOD mouse model is widely reported to be dependent on high-level production by autoreactive CD4+ and CD8+ T cells of interferon-γ (IFN-γ), generally considered a proinflammatory cytokine. However, IFN-γ can also participate in tolerance-induction pathways, indicating it is not solely proinflammatory. This study addresses how IFN-γ can suppress activation of diabetogenic CD8+ T cells. CD8+ T cells transgenically expressing the diabetogenic AI4 T-cell receptor adoptively transferred disease to otherwise unmanipulated NOD.IFN-γnull , but not standard NOD, mice. AI4 T cells only underwent vigorous intrasplenic proliferation in NOD.IFN-γnull recipients. Disease-protective IFN-γ cou

SUBMITTER: Driver JP 

PROVIDER: S-EPMC5319715 | biostudies-literature | 2017 Mar

REPOSITORIES: biostudies-literature