The cytokine receptor IL-23R plays a fundamental role in inflammation and autoimmunity. However, several observations have been difficult to reconcile under the assumption that only Th17 cells critically depend on IL-23 to acquire a pathogenic phenotype. Here, we report that Th1 cells differentiated in vitro with IL-12 + IL-21 show similar levels of IL-23R expression as in pathogenic Th17 cells. We demonstrate that IL-23R is required for Th1 cells to acquire a highly colitogenic phenotype. scRNAseq analysis of intestinal T cells enabled us to identify novel regulators induced by IL-23R-signaling in Th1 cells which differed from those expressed in Th17 cells. The perturbation of one of these regulators (CD160) in Th1 cells inhibited induction of colitis. In this process, we were able to uncouple IL-23R as a purely Th17 cell-specific factor and implicate IL-23R signaling as a pathogenic driver of Th1 cell-mediated tissue inflammation and disease.

中文翻译：

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Th1细胞中致生菌表型的诱导取决于IL-23R信号传导

细胞因子受体IL-23R在炎症和自身免疫中起重要作用。但是，在只有Th17细胞严重依赖IL-23才能获得致病性表型的假设下，很难协调几个观察结果。在这里，我们报道与IL-12 + IL-21体外分化的Th1细胞显示与病原Th17细胞相似的IL-23R表达水平。我们证明IL-23R是Th1细胞获得高致结肠炎表型所必需的。肠道T细胞的scRNAseq分析使我们能够鉴定Th1细胞中由IL-23R信号诱导的新型调控因子，该调控因子与Th17细胞中表达的调控因子不同。Th1细胞中这些调节剂之一（CD160）的扰动抑制了结肠炎的诱导。在这个过程中