LAUSR

Background/Aim: Rheumatoid arthritis (RA) is an autoimmune disease characterized by synovial inflammation and cartilage destruction. Tripartite motif-containing 22 (TRIM22) is involved in intracellular signal transduction, protein regulation, and innate immunity through E3 ubiquitin ligase activity. In this study, we examined the expression of TRIM22 and its potential role in synovial inflammation in RA. Materials and Methods: Human rheumatoid fibroblast-like synoviocytes (RFLS) were cultured and treated with polyinosinic:polycytidylic acid (poly I:C), a toll-like receptor 3 (TLR3) ligand. Poly I:C was applied at different concentrations for different treatment durations. RNA interference was performed by pre-treating RFLS with either non-silencing control small interfering RNA (siRNA) or siRNA targeting TRIM22, interferon β (IFNB), and nuclear factor-kappa B (NFKB) p65. TRIM22 expression in RA synovial tissue was analyzed by immunohistochemistry. Results: TRIM22 expression in RFLS was induced by poly I:C in a concentration and time-dependent manner, and TRIM22 and C-C motif chemokine ligand 5 (CCL5) were regulated by IFN-β and NF-κB pathways. TRIM22 knockdown reduced poly I:C-induced expression of CCL5 and IFN-β. Immunohistochemistry confirmed higher TRIM22 expression in RA synovial tissue compared to osteoarthritis tissue. Conclusion: Treatment of cultured RFLS with a TLR3 agonist led to the upregulation of TRIM22 expression. TRIM22 is regulated through the IFN-β and NF-κB-mediated pathways and TRIM22 positively regulates poly I:C-induced CCL5 and IFN-β expression. TRIM22 may have an important role in synovial inflammation associated with RA.