Abstract

The main aim of this study is to investigate the underlying relationship shared between microRNA-200a (miR-200a) and its link to concentrations of Th17 and Treg cells, mRNA expressions of their specific transcription factors retinoic acid-related orphan receptor γt (RORγt) and head box protein 3 (FOXP3) and relevant cytokines in patients with psoriasis vulgaris (PV). A total of 189 patients previously diagnosed with PV were selected as the experimental group, whilst 109 healthy individuals as the control group. According to the psoriasis area and severity index (PASI), subjects in the experimental group were assigned into the severe group (95 cases) and the moderate group (94 cases). CD4+ T and Th17/Treg cells were extracted. MiR-200a expression and RORγt and FoxP3 mRNA expressions were detected by qRT-PCR. Concentrations of Th17 and Treg cells were measured via flow cytometry. ELISA was conducted for serum IL-17, IL-23 and TGF-β levels. Correlation analysis was completed in accordance with the Pearson method. Compared with the moderate group, higher miR-200a expression, RORγt mRNA expression, percentage of Th17, Th17/Treg ratio and levels of IL-17 and IL-23 exhibited in the severe group, whilst FoxP3 mRNA expression and, percentage of Treg as well as TGF-β were lower. A same trend displayed when comparing the moderate group to the control group. We found that miR-200a expression, percentage of Th17, Th17/Treg ratio, IL-17 and IL-23 levels and RORγt mRNA expression are positively correlated with PASI grade, while the percentage of Treg, TGF-β level and FoxP3 mRNA expression are negatively correlated with PASI grade. The results also displayed that the percentage of Th17, Th17/Treg ratio, IL-17 and IL-23 levels and RORγt mRNA expression are positively correlated with miR-200a expression, while the percentage seen in Treg and TGF-βand FoxP3 mRNA expression are negatively correlated with miR-200a expression. Our results provided a strong evidence that up-regulation of microRNA-200a in CD4+ T cells may induce immune dysfunction through Th17/Treg cells and relevant cytokines in PV patients.

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