TGFβ1 signaling sustains aryl hydrocarbon receptor (AHR) expression and restrains the pathogenic potential of T_H17 cells by an AHR-independent mechanism.

ABSTRACT: The aryl hydrocarbon receptor (AHR) is a transcription factor activated by ligand highly expressed on T_H17 cells, and AHR-deficient CD4⁺ T cells have impaired production of IL-17A and IL-22. Although AHR activation can exacerbate in vivo T_H17 cell-mediated autoimmunity, accumulating data indicate that AHR is a nonpathogenic T_H17 marker. Thus it remains unclear how AHR activation is regulated and impacts on the generation of T_H17 subsets. Here we demonstrated that AHR pathway is activated during in vitro pathogenic T_H17 polarization, but it is quickly downregulated. Under these conditions, additional AHR activation promoted IL-22 but not IL-17A. Interestingly, AHR high sustained expression and IL-17A promotion were only achie

SUBMITTER: de Lima KA 

PROVIDER: S-EPMC6234206 | biostudies-literature | 2018 Nov

REPOSITORIES: biostudies-literature