Recombinant programmed cell death 1 inhibits psoriatic inflammation in imiquimod-treated mice

Abstract

Psoriasis is a common chronic inflammatory skin disease. Programmed cell death ligand 1 (Pd-L1) and programmed cell death 1 (Pd-1) are expressed on immune cells in a number of chronic inflammatory diseases. However, a limited number of studies have investigated the expression and function of the PD-L1 and PD-1 pathway in psoriatic inflammation. The present study used human psoriasis samples and imiquimod-induced murine psoriasis models to investigate the potential role of PD-1 in the modulation of psoriatic inflammation. The results demonstrated that inhibition of Pd-1 function with antibodies promoted psoriasis development. Pd-1-fragment crystallizable (Pd-1-Fc) treatment inhibited psoriatic inflammation and exhibited additive effects with anti-tumor necrosis factor α therapy in imiquimod-induced mouse psoriasis, suggesting that PD-1-Fc treatment may serve as a new therapeutic strategy for psoriasis.