國家衛生研究院 NHRI:Item 3990099045/11390
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    題名: GLK-IKKbeta signaling induces dimerization and translocation of the AhR-RORgammat complex in IL-17A induction and autoimmune disease
    其他題名: GLK-IKKβ signaling induces dimerization and translocation of the AhR-RORγt complex in IL-17A induction and autoimmune disease
    作者: Chuang, HC;Tsai, CY;Hsueh, CH;Tan, TH
    貢獻者: Immunology Research Center
    摘要: Retinoic-acid-receptor-related orphan nuclear receptor γt (RORγt) controls the transcription of interleukin-17A (IL-17A), which plays critical roles in the pathogenesis of autoimmune diseases. Severity of several human autoimmune diseases is correlated with frequencies of germinal center kinase–like kinase (GLK) (also known as MAP4K3)–overexpressing T cells; however, the mechanism of GLK overexpression–induced autoimmunity remains unclear. We report the signal transduction converging on aryl hydrocarbon receptor (AhR)–RORγt interaction to activate transcription of the IL-17A gene in T cells. T cell–specific GLK transgenic mice spontaneously developed autoimmune diseases with selective induction of IL-17A in T cells. In GLK transgenic T cells, protein kinase Cθ (PKCθ) phosphorylated AhR at Ser36 and induced AhR nuclear translocation. AhR also interacted with RORγt and transported RORγt into the nucleus. IKKβ (inhibitor of nuclear factor κB kinase β)–mediated RORγt Ser489 phosphorylation induced the AhR-RORγt interaction. T cell receptor (TCR) signaling also induced the novel RORγt phosphorylation and subsequent AhR-RORγt interaction. Collectively, TCR signaling or GLK overexpression induces IL-17A transcription through the IKKβ-mediated RORγt phosphorylation and the AhR-RORγt interaction in T cells. Our findings suggest that inhibitors of GLK or the AhR-RORγt complex could be used as IL-17A–blocking agents for IL-17A–mediated autoimmune diseases.
    日期: 2018-09-12
    關聯: Science Advances. 2018 Sep 12;4(9):Article number eaat5401.
    Link to: http://dx.doi.org/10.1126/sciadv.aat5401
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=2375-2548&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000449224000027
    Cited Times(Scopus): https://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85053142875
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