Schisandrin B-mediated TH17 cell differentiation attenuates bowel inflammation

The transcription factor STAT3 facilitates naïve CD4+ T cells differentiation into TH17 cells. While, Sch B decreases IL-17A production of CD4+ T cells by targeting STAT3 in vitro and in vivo. TH17 cells promotes the pathogenesis of IBD. Thus, Sch B alleviates IBD through decreasing TH17 cells. [Dis...

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Veröffentlicht in:Pharmacological research 2021-04, Vol.166, p.105459, Article 105459
Hauptverfasser: Ma, Zeyu, Xu, Gang, Shen, Yingying, Hu, Shufang, Lin, Xia, Zhou, Jun, Zhao, Wei, Liu, Jian, Wang, Jiaoli, Guo, Jufeng
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Sprache:eng
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Zusammenfassung:The transcription factor STAT3 facilitates naïve CD4+ T cells differentiation into TH17 cells. While, Sch B decreases IL-17A production of CD4+ T cells by targeting STAT3 in vitro and in vivo. TH17 cells promotes the pathogenesis of IBD. Thus, Sch B alleviates IBD through decreasing TH17 cells. [Display omitted] •Schisandrin B alleviates DSS-induced acute and chronic colitis.•Schisandrin B alleviates CD4+CD45RBhigh T cell-induced colitis.•Schisandrin B protects mice from colitis by targeting TH17 cells.•Schisandrin B decreases TH17 cell differentiation in a STAT3 dependent manner.•Schisandrin B inhibited human TH17 cell differentiation in vitro. Schisandrin B (Sch B) is the major active constituent of the traditional Chinese medicine Schisandra chinensis and has anti-inflammatory activity, but the target of Sch B remains unclear. T helper 17 (TH17) cells have been involved in the pathogenesis of many autoimmune and inflammatory diseases. Here, we showed that Sch B could decrease IL-17A production of CD4+ T cells by targeting STAT3 in vitro. Importantly, Sch B has therapeutic effects on DSS-induced acute and chronic colitis, CD4+CD45RBhigh T cell-induced colitis. Furthermore, we identified TH17 cells as the direct target of Sch B for mediating its anti-inflammatory activity. Sch B could serve as a lead for developing new therapeutics against TH17 cells or IL-17A cytokine-driven diseases.
ISSN:1043-6618
1096-1186
DOI:10.1016/j.phrs.2021.105459