The Role Of MicroRNA-210in The Regulation Of T Cell Activation And The Pathogenesis Of Psoriasis Vulgaris

Objective. Psoriasis vulgaris(PV) is a common, chronic, recurred dermatological disorder, and charactered by erythema scaled, affecting the appearance and emotion of patients. About the pathogenesis, PV is considered as a immune-mediated autoinflammatory disease, and the progression is linked to the activated effector T cells and the dysfunction of regulatory T cells. A growing body of research demonstrated microRNAs played a crucial role in the activation and dysfunction of CD4+lymphocytes. Previous microRNA microarray studies by our group showed that the expression of microRNA-210(miRNA-210) was upregulated significantly in the PBMCs of patients with PV compared with healthy controls. In this study, we investigatedthe effect and mechanism of miR-210in the immunological dysregulation of psoriasis vulgaris (PV), in order to provide new ideas for pathogenesis of psoriasis vulgaris.Methods. CD4+T cells were isolated from peripheral blood of18PV patients and18healthy individuals by magnetic beads. The expression levels of miR-210in CD4+T cells were detected by real-time polymerase chain reaction (RT-PCR). Target genes of miR-210were predicted by bio-informatics softwares including Mirbase/Targetscans/PicTar. Potential target genes were verified using luciferase reporter gene assays. RT-PCR was performed to evaluate the mRNA levels of target genes, and Western blot was performed to determine the protein level of target genes. CD4+T cells from healthy individuals or PV patients were transfected with miR-210mimics or inhibitors using the human T cell nucleofector Kit. The levels of cytokines in the supernatant of cells culture were detected using enzyme-linked immunosorbent assay (ELISA).Result. The expression of miR-210is up-regulated significantly in the CD4+T cells from PV patients compared to healthy controls. According to prediction of bio-informatic softwares and luciferase reporter gene assay, we confirmed that FOXP3is a target gene of miR-210, which is the key transcription factor of regulatory T cells. The expression of FOXP3was down-regulated in the CD4+T cells from PV patients, and are significantly negative correlated with the expression levels of miR-210. When miR-210mimic was transfected into normal CD4+T cells, FOXP3expression was down-regulated compared with negative controls, meanwhile the levels of IL-10and TGF-β were decreased and the level of IFN-γ was increased. When miR-210inhibitor was transfected into PV CD4+T cells, FOXP3expression were up-regulated, at the same time the levels of IL-10and TGF-β were increased and the level of IFN-y was decreased.Conclusion. Our data demonstrate that expression of miR-210is upregulated in CD4+T cells from patients with PV. Upregulation of miR-210inhibits FOXP3expression, contributing to CD4+T cells abnormal activation and increased inflammatory factors. These data suggest that miR-210may play a important role in the development and progression of PV.