This study investigates the role of dermal γδ T cells in skin inflammation, particularly in psoriasis. The authors found that IL-23 primarily stimulates dermal γδ T cells to produce IL-17, which is crucial for disease progression. Dermal γδ T cells express the IL-23 receptor (IL-23R), RORγt, and various chemokine receptors. IL-17 production from these cells is independent of αβ T cells. In mice, IL-23-induced skin inflammation and epidermal hyperplasia were significantly reduced in T cell receptor δ deficient (Tcrδ−/−) and IL-17 receptor deficient (Il17ra−/−) mice. Additionally, imiquimod-induced skin pathology was significantly decreased in Tcrδ−/− mice. In human psoriatic skin, γδ T cells were significantly increased and produced large amounts of IL-17 upon IL-23 stimulation. These findings suggest that IL-23-responsive dermal γδ T cells are major IL-17 producers in the skin and may represent a novel target for treating psoriasis.This study investigates the role of dermal γδ T cells in skin inflammation, particularly in psoriasis. The authors found that IL-23 primarily stimulates dermal γδ T cells to produce IL-17, which is crucial for disease progression. Dermal γδ T cells express the IL-23 receptor (IL-23R), RORγt, and various chemokine receptors. IL-17 production from these cells is independent of αβ T cells. In mice, IL-23-induced skin inflammation and epidermal hyperplasia were significantly reduced in T cell receptor δ deficient (Tcrδ−/−) and IL-17 receptor deficient (Il17ra−/−) mice. Additionally, imiquimod-induced skin pathology was significantly decreased in Tcrδ−/− mice. In human psoriatic skin, γδ T cells were significantly increased and produced large amounts of IL-17 upon IL-23 stimulation. These findings suggest that IL-23-responsive dermal γδ T cells are major IL-17 producers in the skin and may represent a novel target for treating psoriasis.