The aryl hydrocarbon receptor (AHR) is a transcription factor activated by ligand highly expressed on T 17 cells, and AHR-deficient CD4 T cells have impaired production of IL-17A and IL-22. Although AHR activation can exacerbate in vivo T 17 cell-mediated autoimmunity, accumulating data indicate that AHR is a nonpathogenic T 17 marker. Thus it remains unclear how AHR activation is regulated and impacts on the generation of T 17 subsets. Here we demonstrated that AHR pathway is activated during in vitro pathogenic T 17 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 achieved when TGFβ1 was present in the culture. In addition to the effect on AHR regulation, TGFβ1 presented a dual role by simultaneously suppressing the T 17 pathogenic phenotype acquisition. This latter effect was independent of AHR stimulation, since its activation did not confer a T 17 anti-inflammatory profile and Ahr cells did not upregulate any T 17 pathogenic marker. Through the use of EAE model, we demonstrated that AHR is still functional in encephalitogenic CD4 T cells and the adoptive transfer of Ahr T 17 cells to recipient mice resulted in milder EAE development when compared to their WT counterparts. Altogether, our data demonstrated that although AHR is highly expressed on in vitro-generated nonpathogenic T 17 cells, its ligation does not shift T 17 cells to an anti-inflammatory phenotype. Further studies investigating the role of AHR beyond T 17 differentiation may provide a useful understanding of the physiopathology of autoimmune diseases.