Alloferon and IL-22 receptor expression regulation on the pathogenesis of imiquimod-induced psoriasis

We investigated the regulatory role of alloferon in the development of psoriasis in an imiquimod (IMQ)-induced psoriasis model through the regulation of IL-22Rα expression. Psoriasis is an immune-mediated inflammatory skin disease. IL-22, a proinflammatory cytokine, is implicated in psoriasis pathogenesis; however, there is currently no established biological treatment targeting IL-22 or its receptor, IL-22Rα. Alloferon is a short peptide that has an anti inflammatory effect on skin disorders; however, little is known about its anti-inflammatory activity in psoriasis. This study demonstrate that alloferon could be an effective potential drug for the treatment of psoriasis by interrupting IL-22 signaling and factors related to skin inflammation. Male B6 wild-type (WT) mice and IL-22Rα knock-out (KO) mice (n=4 per group) were used to compare the effects of IMQ-induced psoriasis-like inflammation. IMQ cream (83.3 mg, 5%) was applied daily to the dorsal skin and ears of both groups from day 1 to day 7, with treatment mice receiving either vehicle cream or alloferon cream 6 hours after IMQ application. Total RNA was extracted from the dorsal skin of WT and KO mice for comparative transcriptomic analysis.