Rekik et al. (177) demonstrated that transcription of TGF-β1 target genes are impaired in CD3+ T cells of active SLE patients and this impaired response to TGF-β1 is associated with an overexpression of IL-22 in SLE patients suggesting that excessive activation of AHR pathway could inhibit the immunosuppressive effects of TGF-β1 leading to exacerbated SLE. Here, IL22 is linked to systemic lupus erythematosus.