Abstract:

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）. Conclusion Elevated expression of miR-155 in RA patients may mediate the differentiation of CD4⁺ T cells into Th17 cells through the SOCS1/STAT3 pathway， contributing to the imbalance of Th17/Treg cells in peripheral blood of RA patients.

Key words: rheumatoid arthritis, miR-155, suppress of cytokine signaling 1 （SOCS1）, Th17/Treg imbalance