miR-452-5p promotes systemic lupus erythematosus-induced inflammatory responses by downregulating RBL2 and impairing Treg development.

Systemic lupus erythematosus (SLE) is a complex autoimmune disease. Studies have reported that miR-452-5p is highly expressed in SLE, while RBL2 is downregulated. This study aims to investigate the diagnostic value of miR-452-5p in distinguishing healthy controls from SLE patients and its potential regulatory mechanisms in SLE. A total of 114 patients with SLE were included in this study. The expressions of miR-452-5p, RBL2, Foxp3, CD4, CD25, RORC and IL-17 A were detected by RT-qPCR. The diagnostic value of miR-452-5p was analyzed by ROC. Cell detection included proliferation and apoptosis experiments, which were determined by CCK-8 method and flow cytometry respectively. ELISA was used to determine the contents of IFN-γ, TNF-α, IL-6, TGF-β1 and IL-10 in the cell supernatant. DLR verified the binding relationship between miR-452-5p and RBL2. Compared with the healthy control group, the expression of miR-452-5p was upregulated. Its diagnostic value for SLE reaches 0.902. miR-452-5p targets and regulates RBL2. Excessive proliferation of PBMCs, reduced apoptosis and imbalance of Treg/Th17. After inhibiting miR-452-5p, the RBL2 level increased, the PBMC proliferation decreased, and apoptosis increased. The Treg marker genes Fxop3, CD4 and CD25 levels increased, while the Th17 marker genes RORC and IL-17 A levels decreased. Inhibiting RBL2 can reverse the above changes. miR-452-5p is expected to become a novel biomarker for SLE. miR-452-5p may affect the proliferation and apoptosis of PBMC and the balance of Treg/Th17 cells by targeting RBL2 mRNA, and participate in the immunopathological process of SLE.