Immunoregulatory Impact of miR-124 and miR-223 on Some Immunological Parameters in Rheumatoid Arthritis

Rheumatoid arthritis (RA) is a long-lasting autoimmune disorder that causes inflammation of the synovium and the destruction of joints. This study evaluated the expression of miR-124 and miR-223 in RA patients and their association with key inflammatory markers: sCD28, IL-6, IL-17A, IL-40, MCP-1, and VEGF. One hundred eighty participants were enrolled, including 120 RA patients (newly diagnosed and biologically treated) and 60 healthy controls. Serum cytokine levels were measured using sandwich ELISA, and miRNA expression was quantified by qRT-PCR. Results revealed significant, distinct yet overlapping dysregulation of miR-124 and miR-223 in RA patients in comparison to controls, influenced by inflammatory status, therapeutic intervention, and patient-specific factors. These alterations correlated positively with raised serum levels of IL-6, IL-17A, and VEGF, indicating active inflammation, immune activation, and angiogenesis. Biological therapy significantly reduced miRNA dysregulation and inflammatory marker levels, reflecting effective disease control. The expression profiles of miR-124 and miR-223 closely reflected both inflammatory activity and therapeutic response. The correlation between expression of miR-223 and pro-inflammatory mediators reinforce its role in supporting T-cell activation and immunogenic signaling, while the contrary pattern of miR-124 indicates a regulatory role in modulating inflammatory cascades and angiogenesis. The immunological indicators sCD28, MCP-1, IL-40, and VEGF illuminate the reciprocal influence of immune activation, chemotaxis, and vascular remodeling in the pathogenesis of RA. The study's outcomes substantiate miR-124 and miR-223 as consistent diagnostic biomarkers of RA. Moreover, the essential roles of related immunological markers in disease activity and therapeutic response. This study contributes to enhancing the importance of using miRNA in modifying the immune reaction by influencing the concentration and function of inflammatory mediators to reduce the development and severity of RA and enhances the therapeutic response, with the feasibility of using them as diagnostic parameters and therapeutic targets.