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- W4313387722 abstract "Abstract It has been recently found that mice lacking IL-12 specific receptor subunit, namely IL-12Rβ2, developed more severe clinical and pathological signs of in experimental autoimmune encephalomyelitis (EAE), an animal model of human multiple sclerosis. However, whether this phenomenon is also true in other autoimmune disorders and the mechanism underlying this phenomenon is not known. We in the present study have shown that IL-12Rβ2-deficient mice also develop earlier and more severe disease in the streptozotocin-induced model of diabetes, indicating a universal susceptibility to autoimmune diseases in IL-12Rβ2-deficient mice. IL-12Rβ2-deficient mice exhibited significantly higher effector T cell proliferative responses not only to autoantigens, but also to non-specific stimuli. Compared to wild type mice, IL-12Rβ2-deficient mice exhibited significantly reduced capacity to develop regulatory T cells (Treg) in vivo in the thymus and in vitro upon stimulation with TGF-β. Further, naturally-occurring Treg cells from these mice were less functional in suppressing effector T cells. These findings indicated that signal via IL-12Rβ2 plays an essential in developing high quantity and quality of Treg cells, which confers a novel mechanism underlying the regulation of autoimmune diseases by the IL-12 pathway." @default.
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- W4313387722 date "2007-04-01" @default.
- W4313387722 modified "2023-10-16" @default.
- W4313387722 title "Signal via IL-12Rβ2 plays an essential role in the development of CD4+CD25+ regulatory T cells (129.27)" @default.
- W4313387722 doi "https://doi.org/10.4049/jimmunol.178.supp.129.27" @default.
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