LAUSR

Abstract Psoriasis is an autoimmune disease that is characterized by discolored, scaled patches of skin. Clinically, it is found that psychological factors often induce or aggravate the disease. Current research suggests that the pathogenesis of psoriasis involves the nervous and immune systems. This article reviews how neuropeptides secreted by nerve fibers affect dendritic cells in psoriasis. In this review, we describe that the neuropeptides calcitonin gene-related peptide, substance P, and vasoactive intestinal peptide can act on dendritic cells and participate in the pathogenesis of psoriasis. These neuropeptides can affect the secretion of interleukin (IL)-12 and IL-23 by dendritic cells, which stimulate T helper (Th)1, Th17, and Th22 cells to produce immune responses and cause the manifestation of psoriasis. The application of neuropeptide inhibitors can improve the skin lesions of psoriasis, which has been confirmed in clinical trials. Therefore, neuroimmune response may be a new direction to develop new drug treatments and perspectives in the development of psoriasis.