IL-36 is a recent new member of IL-1 family cytokines, which has shown a close association with inflammatory diseases including pustular psoriasis and inflammatory bowel colitis. IL-36 cytokines are composed of IL-36α, IL36β, IL-36γ, and they enhance cytokine production from immune-related cells including dendritic cells and T cells, and keratinocytes. Among these, we found that IL-36a is highly expressed in inflamed mouse skin in IMQ-induced psoriasis model, but the role of IL-36α in vivo was not clear. Here, we generated IL-36α KO mice and found that IL-36α KO mice developed significantly milder dermatitis in IMQ-induced psoriasis. To reveal the key player cells in this phenotype, we applied bone marrow cell transfer model and found out that IL-36α expression in skin-resident cells, not in hematopoietic cells including immune-related cells, is important for the pathogenesis of dermatitis. We found that the expression of activation markers and chemokines was enhanced in skin-reident cells. Interestingly, we found that IL-36α deficiency ameliorated symptoms in IMQ-induced dermatitis even in microflora-normalized housing sytem, suggesting that IL-36α function can overcome the effect of microflora. We believe that IL-36α is a promising target for the development of therapeutics