Open AccessRecombinant programmed cell death 1 inhibits psoriatic inflammation in imiquimod‑treated mice
Author(s) -
Shichun Peng,
Mei Cao,
Xiaoying Sun,
Yajun Zhou,
ChuYen Chen,
Tian Ma,
Hongjin Li,
Bin Li,
Bo Zhu,
Xin Li
Publication year - 2020
Publication title -
international journal of molecular medicine
Language(s) - Uncategorized
Resource type - Journals
SCImago Journal Rank - 1.048
H-Index - 90
eISSN - 1791-244X
pISSN - 1107-3756
DOI - 10.3892/ijmm.2020.4612
Subject(s) - psoriasis , imiquimod , inflammation , tumor necrosis factor alpha , medicine , immunology , programmed cell death , apoptosis , immune system , cancer research , biology , biochemistry
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.