The role of miR-3917/HLA-DRB1 in Th17 cell differentiation affects chronic periodontitis

Chronic periodontitis (CP) is an inflammatory-destructive disease, and Th17 cells play a vital role in driving and regulating CP. This study aimed to confirm the influence of miR-3917/HLA-DRB1 in the differentiation of CD4⁺ T cells to Th17 cells. The differentially expressed microRNAs (miRNAs) in CP were screened from the Gene Expression Omnibus (GEO) database, and then the target gene of miR-3917 was confirmed by using the RT-qPCR and Dual-Luciferase assay. clinical data of patients with CP and healthy individuals were collected, and intergroup comparisons were performed using ROC and logistic regression analysis. A CD4⁺T cell differentiation model was established to explore the role of the miR-3917/HLA-DRB1 axis in regulating CD4⁺T cell differentiation into Th17 cells. STAT3 and RORγt levels were detected by RT-qPCR and WB. Production of IL-17 and IL-21 was determined by ELISA kits. MiR-3917 upregulation and HLA-DRB1 downregulation were detected in patients with CP. Overexpression of miR-3917 promoted the differentiation of CD4⁺T cells toward Th17 cells, boosted the secretion of IL-17 and IL-21, and elevated the levels of STAT3 and RORγt, whereas inhibition of miR-3917 exerted the opposite effects. Rescue experiment confirmed that miR-3917 increased Th17 cell differentiation by directly targeting and regulating HLA-DRB1. MiR-3917 downregulated HLA-DRB1, thereby promoting Th17 cell differentiation and ultimately aggravating inflammation. These findings suggested that miR-3917 may be involved in CP pathogenesis and might serve as a potential diagnostic biomarker for CP.