Acting in concert with TGF-β, interleukin-6 (IL-6) signaling induces T helper 17 (T_H17) cell development by programming T_H17-related genes via signal transducers and activators of transcription 3 (STAT3). A role for IL-6 signaling beyond the inductive phase of T_H17 cell development has not been defined because IL-23 signaling downstream of T_H17 cell induction also activates STAT3 and is thought responsible for T_H17 cell maintenance. Here, we find that IL-6 signaling is required for both induction and maintenance of mouse T_H17 cells; IL-6Rα–deficient T_H17 cells rapidly lost their T_H17 phenotype and did not cause disease in two models of colitis. Cotransfer of wild-type T_H17 cells with IL-6Rα–deficient T_H17 cells induced colitis but was unable to rescue phenotype loss of the latter. High IL-6 expression in the colon promoted classic, or cis, rather than transreceptor signaling that was required for maintenance of T_H17 cells. Thus, ongoing classic IL-6 signaling underpins the T_H17 program and is required for T_H17 cell maintenance and function.

白细胞介素 6 (IL-6) 与 TGF-β 协同作用，通过信号转导子和转录激活因子 3 (STAT3) 对 T _H 17 相关基因进行编程，从而诱导 T 辅助细胞17 (T _{H 17) 发育。IL-6 信号传导在 T H} 17 细胞发育的诱导期之外的作用尚未确定，因为 T _H 17 细胞诱导下游的 IL-23 信号传导也激活 STAT3，并被认为负责 T _H 17 细胞的维持。在这里，我们发现 IL-6 信号是诱导和维持小鼠 T _H 17 细胞所必需的。IL-6Rα 缺陷型 T _H 17 细胞迅速失去其 T _H17 表型，并且在两种结肠炎模型中均未引起疾病。野生型 T _H 17 细胞与 IL-6Rα 缺陷型 T _H 17 细胞的共转移诱导结肠炎，但无法挽救后者的表型损失。_{结肠中的高 IL-6 表达促进了经典或顺式，而不是维持 T H} 17 细胞所需的跨受体信号传导。因此，正在进行的经典 IL-6 信号传导支持 T _H 17 程序，并且是 T _H 17 细胞维持和功能所必需的。