The skin is an immune barrier which has the difficult task of maintaining tissue homeostasis while interacting with the outside world. Dysregulation of skin immune cells can lead to cutaneous inflammatory diseases such as psoriasis. Central to the pathogenesis of psoriasis is the IL-23/IL-17 immune axis. Specifically, it has been shown that production of IL-23 by skin-resident myeloid cells drives the expansion of IL-17 secreting T cells, which promotes skin inflammation. However, the initiating factors that activate this inflammatory immune axis are unknown. Prostaglandin E2 (PGE2) is an important member of the eicosanoid family of lipid mediators that modulates inflammation in a tissue- and cell-specific manner. Although increased PGE2 is observed in the skin of psoriasis patients and has been previously shown to amplify the IL-23/IL-17 axis during neuroinflammatory disease and allergy, its role in cutaneous immunity has not been closely examined. We hypothesized that PGE2 enhances IL-23-driven IL-17 production by gd T cells, a subset of innate lymphocytes implicated in psoriatic disease. Our results indicate that PGE2 increases IL-17 transcription and secretion by murine gd T cells in vitro in a time and dose-dependent manner. In addition, PGE2 activity is mediated through the prostanoid receptors EP2 and EP4 expressed by gd T cells and selectively amplifies IL-17A and F expression without increasing IL-22, a cytokine usually co-produced by IL-17 producing cells. Using gain and loss of function strategies in vivo, we additionally observed that PGE2 amplified IL-17-driven psoriasiform inflammation. Altogether, our results show a new role for PGE2 in regulating the innate immune IL-23/IL-17 axis of the skin.