Abstract
Psoriasis vulgaris (PV) is a chronic inflammatory and T cell-mediated autoimmune skin disease. An immune dysfunction that is manifested by abnormally activated T cells and defective regulatory T (Treg) cells may play an important role in the pathogenesis of PV. However, the precise mechanism of the immune dysfunction in PV patients still remains unclear. In this study, we found that miR-210 expression is increased significantly in CD4(+) T cells from patients with PV and confirmed that FOXP3 is a target gene of miR-210. We also found that overexpression of miR-210 inhibits FOXP3 expression and impairs the immunosuppressive functions of Treg cells in CD4(+) T cells from healthy controls. In contrast, inhibition of miR-210 increases FOXP3 expression and reverses the immune dysfunction in CD4(+) T cells from patients with PV. Our data demonstrates that increased miR-210 induces immune dysfunction via by FOXP3 in CD4(+) T cells from patients with PV.