[Inflammation caused by different immune cell subsets is involved in bone destruction of rheumatoid arthritis]

Objective To observe the relationship of rheumatoid arthritis (RA) bone destruction with T cells, regulatory T cells (Tregs), CD19⁺ B cells and immune inflammation. Methods The study enrolled randomly 20 RA patients (RA group) and 20 normal controls (NC group). Bone mineral density was measured by DXEA dual energy X-ray bone densitometer. The serum levels of γ-interferon (IFN-γ) of Th1 cells, interleukin-4 (IL-4) of Th2 cells, IL-17, type I procollagen amino terminal propeptide (PINP), type I collagen carboxy terminal peptide (CTx), receptor activator of NF-κB ligand (RANKL) and osteoprotectin (OPG) were detected by ELISA. T-cell subsets, Tregs, CD19⁺ B cells in peripheral blood were measured by flow cytometry. Spearman method was used to analyze the correlations of T cells, Treg and CD19⁺ B cells with bone density and Th1 and Th2 cytokines. Results The bone mineral density T value of the RA group was lower than that of the NC group. The bone mineral density T value of the double forearm was lower than that of the lumbar spine in the RA group. Compared with the NC group, the expression of IFN-γ, IL-17, Th1/Th2 cells, CTx, RANKL increased, and IL-4, PINP decreased in the RA group. Compared with the NC group, the expression of CD4⁺/CD8⁺ T cells, CD19⁺ B cells increased, and CD8⁺ T cells, CD4⁺CD25⁺ Tregs decreased in the RA group. Correlation analysis showed that CD8⁺ T cells were positively correlated with Th1/Th2 cells and IL-17, while CD4⁺ CD25⁺ Tregs were negatively correlated with CTx, and CD19⁺ B cells were negatively correlated with OPG in RA. Conclusion T cells and CD19⁺ B cells may participate in the process of bone destruction in RA by mediating inflammatory immunity.