T_H17 cells require ongoing classic IL-6 receptor signaling to retain transcriptional and functional identity.

ABSTRACT: 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-d

SUBMITTER: Harbour SN 

PROVIDER: S-EPMC7843024 | biostudies-literature | 2020 Jul

REPOSITORIES: biostudies-literature