Abstract Recently, others and we have identified a unique subset of γδ T cells in dermis that is capable of producing IL-17. Dermal γδ T cells have been demonstrated to play a critical role in the psoriasis pathogenesis. However, it is still unclear how these cells are developed and regulated. In this study, we found that dermal γδ T cells were mainly developed from the thymus. Surprisingly, there is also an extrathymic pathway for these cells development as our data showed that bone marrow cells alone could also reconstitute the dermal γδ T cells in the mice absence of thymus (Nude mice). Although most of dermal γδ T cells are skin bona-fide residents, there were a part of γδ T cells migrated from the periphery. Such trafficking process required chemokine receptor 6. In the periphery, we found that both IL-23 and IL-1β promoted dermal γδ T cells proliferation. However, IL-23-induced dermal γδ T cell proliferation was mainly dependent on IL-1β. Additionally, IL-1β synergized with IL-23 to produce large amounts of IL-17 by dermal γδ T cells. Moreover, mice with IL-1RI deficiency had significantly decreased epidermal thickness and neutrophil infiltration induced by IL-23 or Imiquimod. Taken together, we demonstrate the development, peripheral trafficking and regulation of dermal γδ T cells, which provides new insights into understanding the biology of this newly discovered cell population and implies new mechanisms involved in the pathogenesis of skin inflammation such as psoriasis.