MiR-155 regulates inflammatory responses and Th17/Treg imbalances in rheumatoid arthritis through the SOCS1/STAT3 pathway.

Objective This research aimed to investigate the expression and mechanism of miR-155 and suppressor of cytokine signaling 1 (SOCS1) in rheumatoid arthritis (RA). Methods RT-PCR and flow cytometry were applied to detect the expression differences of miR-155, Th17, and Treg cells in peripheral blood of RA patients (RA group) and control group (HC group). Bioinformatics analysis and dual-luciferase reporter assay were conducted to investigate the regulatory relationship between miR-155 and SOCS1. CD4+T cells were isolated from peripheral blood of RA patients and transfected with miR-155 inhibitor, si-SOCS1, and their respective negative control sequences, and divided into four groups: miR-NC group, miR-155 inhibitor group, miR-155 inhibitor+ si-NC group, and miR-155 inhibitor+si-SOCS1 group. The cells were treated with Th17-inducing differentiation medium, and flow cytometry was used to determine the ratio of Th17 cells in each group of CD4+T cells. Western blot was used to determine the ratio of p-STAT3/STAT3 in the cells. Results Compared to the HC group, RA patients showed increased expression of miR-155 and Th17 ratio (P < 0.01), and decreased Treg cell ratio (P < 0.01). MiR-155 could target and inhibit the expression of SOCS1. Compared to the miR-NC group, the miR-155 inhibitor group, miR-155 inhibitor+si-NC group, and miR-155 inhibitor+si-SOCS1 group showed decreased Th17 ratio and p-STAT3/STAT3 ratio (P < 0.01). Compared to the miR-155 inhibitor group, the miR-155 inhibitor+ si-SOCS1 group exhibited increased Th17 ratio and p-STAT3/STAT3 ratio in CD4+T cells (P < 0.05). Conclusio through the SOCS1/STAT3 pathway, contributing to the imbalance of Th17/Treg cells in peripheral blood of RA patients. [ABSTRACT FROM AUTHOR]