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  • 1
    Publication Date: 2019
    Description: 〈p〉IL-6/STAT3 signaling is known to initiate the T〈sub〉H〈/sub〉17 differentiation program, but the upstream regulatory mechanisms remain minimally explored. Here, we show that Cxxc finger protein 1 (Cxxc1) promoted the generation of T〈sub〉H〈/sub〉17 cells as an epigenetic regulator and prevented their differentiation into T〈sub〉reg〈/sub〉 cells. Mice with a T cell–specific deletion of Cxxc1 were protected from experimental autoimmune encephalomyelitis and were more susceptible to 〈i〉Citrobacter rodentium〈/i〉 infection. Cxxc1 deficiency decreased IL-6Rα expression and impeded IL-6/STAT3 signaling, whereas the overexpression of IL-6Rα could partially reverse the defects in 〈i〉Cxxc1〈/i〉-deficient T〈sub〉H〈/sub〉17 cells in vitro and in vivo. Genome-wide occupancy analysis revealed that Cxxc1 bound to 〈i〉Il6r〈/i〉α gene loci by maintaining the appropriate H3K4me3 modification of its promoter. Therefore, these data highlight that Cxxc1 as a key regulator governs the balance between T〈sub〉H〈/sub〉17 and T〈sub〉reg〈/sub〉 cells by controlling the expression of IL-6Rα, which affects IL-6/STAT3 signaling and has an impact on T〈sub〉H〈/sub〉17-related autoimmune diseases.〈/p〉
    Electronic ISSN: 2375-2548
    Topics: Natural Sciences in General
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