The study investigates the role of the aryl hydrocarbon receptor (AhR) in TH17-cell-mediated autoimmunity and its link to environmental toxins. AhR is a ligand-dependent transcription factor known for mediating the toxicity of dioxin. The research shows that AhR expression is restricted to the TH17 subset of CD4 T cells and its activation results in the production of the TH17 cytokine IL-22. AhR is also expressed in human TH17 cells. Activation of AhR during TH17 development increases the proportion of TH17 cells and their cytokine production. AhR-deficient mice can develop TH17 responses but fail to produce IL-22 and show reduced TH17 development when exposed to AhR ligands. AhR activation during experimental autoimmune encephalomyelitis (EAE) causes accelerated onset and increased pathology in wild-type mice but not in AhR-deficient mice. The findings suggest that AhR ligands may contribute to the development of autoimmune diseases.The study investigates the role of the aryl hydrocarbon receptor (AhR) in TH17-cell-mediated autoimmunity and its link to environmental toxins. AhR is a ligand-dependent transcription factor known for mediating the toxicity of dioxin. The research shows that AhR expression is restricted to the TH17 subset of CD4 T cells and its activation results in the production of the TH17 cytokine IL-22. AhR is also expressed in human TH17 cells. Activation of AhR during TH17 development increases the proportion of TH17 cells and their cytokine production. AhR-deficient mice can develop TH17 responses but fail to produce IL-22 and show reduced TH17 development when exposed to AhR ligands. AhR activation during experimental autoimmune encephalomyelitis (EAE) causes accelerated onset and increased pathology in wild-type mice but not in AhR-deficient mice. The findings suggest that AhR ligands may contribute to the development of autoimmune diseases.