IL-17 is a proinflammatory cytokine required for the body protection against fungi and bacteria. Dysregulated production of IL-17 can lead to the development of various autoimmune and inflammatory diseases including psoriasis. Although the major attentions have been paid to IL-17- producing helper T cells in psoriasis pathogenesis, the evidence is being accumulated that γδT cells are involved with the development of psoriasis as a primary source of IL-17 in the affected skin. We have investigated the regulatory mechanism of IL-17-producing γδT cells (γδ17) and its association with psoriasis. Herein, we report that a nuclear receptor, REV-ERB, negatively regulates the activation of γδ17 and the topical application of a synthetic REV-ERB ligand can attenuate the inflammatory symptoms of psoriasiform dermatitis in mice. In addition, γδ17 regulation through a novel cytokine and its involvement with psoriasis pathogenesis will be reported.