IL22 and psoriasis: NE receptors on T‐cell surfaces respond to catecholamines.[43, 44] In vitro, NE supplementation drives Th17 T‐lymphocyte polarization, as indicated by increased IL‐17A and IL‐22 expression.[45] In the pathogenesis of psoriasis, IL‐17 and IL‐22 secreted by cutaneous γδT cells induce inflammatory cell recruitment in the skin and abnormal keratinocyte proliferation.[46, 47, 48, 49] In this study, we elucidated the mechanism that catecholamines directly affect another type 17 immune response of γδT cells, but not Th17 cells.