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- W2083040532 abstract "IFN-γ is essential for idiopathic and murine mercury-induced systemic autoimmunity (mHgIA), and heterozygous IFN-γ+/− mice also exhibit reduced disease. This suggests that blocking specific IFN-γ-related pathways that may only partially inhibit IFN-γ production or function will also suppress autoimmunity. To test this hypothesis, mice deficient in genes regulating IFN-γ expression (Casp1, Nlrp3, Il12a, Il12b, Stat4) or function (Ifngr1, Irf1) were examined for mHgIA susceptibility. Absence of either Ifngr1 or Irf1 resulted in a striking reduction of disease, while deficiency of genes promoting IFN-γ expression had modest to no effect. Furthermore, both Irf1− and Ifng-deficiency only modestly reduced the expansion of CD44hi and CD44hiCD55lo CD4+ T cells, indicating that they are not absolutely required for T cell activation. Thus, there is substantial redundancy in genes that regulate IFN-γ expression in contrast to those that mediate later signaling events. These findings have implications for the therapeutic targeting of IFN-γ pathways in systemic autoimmunity." @default.
- W2083040532 created "2016-06-24" @default.
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- W2083040532 date "2012-12-01" @default.
- W2083040532 modified "2023-09-29" @default.
- W2083040532 title "Definition of IFN-γ-related pathways critical for chemically-induced systemic autoimmunity" @default.
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- W2083040532 doi "https://doi.org/10.1016/j.jaut.2012.04.003" @default.
- W2083040532 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3570757" @default.
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