Tyrosine phosphatase SHP2 exacerbates psoriasis-like skin inflammation in mice via ERK5-dependent NETosis.

ABSTRACT: Psoriasis is a chronic inflammatory skin disease, often accompanied by increased infiltration of immune cells, especially neutrophils. However, the detailed mechanism of the neutrophil function in psoriasis progression remains unclear. Here, we found that both Src homology-2 domain-containing protein tyrosine phosphatase-2 (SHP2) and neutrophils were highly correlated to developing psoriasis by single-cell ribonucleic acid (RNA) sequencing and experiment verification. The deficiency of SHP2 in neutrophils significantly alleviated psoriasis-like phenotype in an imiquimod-induced murine model. Interestingly, high levels of neutrophil extracellular traps (NETs) were produced in the inflamed lesions of psoriatic patients. In addition, imiquimod-induced psoriasis-like symptoms were remarkably a

SUBMITTER: Ding Y 

PROVIDER: S-EPMC8906448 | biostudies-literature | 2022 Mar

REPOSITORIES: biostudies-literature