EXPRESSION LEVELS OF ENDOSOMAL TOLL-LIKE RECEPTORS (TLRs) IN RHEUMATOID ARTHRITIS: A LINK BETWEEN TLR7, TLR9, AND INFLAMMATORY BIOMARKERS WITH DISEASE ACTIVITY SCORE

Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by synovial inflammation, joint damage, and functional impairment. Recent studies highlighted the role of Toll-like receptors (TLRs), particularly TLR7 and TLR9, in RA pathogenesis through innate immune activation and interferon-alpha (IFN-α) production. This case-control study assessed TLR7 and TLR9 expression in 60 RA patients and 30 healthy controls, alongside serum IFN-α levels and disease activity (DAS28). Blood samples were processed for RNA extraction and cDNA synthesis. Gene expression was quantified via RT-qPCR, and IFN-α levels measured by ELISA. RA patients showed significantly increased TLR7 (1.99-fold, p = 0.005) and TLR9 (1.42-fold, p = 0.024) expression compared to healthy controls, as determined by the Mann–Whitney U test. A strong positive correlation was observed between their expression levels (ρ = 0.893, p ≤ 0.001), indicating shared co-regulatory mechanisms. IFN-α levels were also significantly elevated in RA patients (p ≤ 0.001). However, correlations between TLR7 expression and IFN-α (ρ = –0.047, p = 0.804) or DAS28 (ρ = 0.148, p = 0.435) were weak and not statistically significant. Similarly, TLR9 expression showed weak, non-significant correlations with IFN-α (ρ = 0.007, p = 0.969) and DAS28 (ρ = 0.161, p = 0.396). Likewise, no significant link was found between age and disease activity. These results suggest that while TLR7, TLR9, and IFN-α are elevated in RA, their direct association with disease activity may be limited, highlighting the complexity of immune regulatory networks in RA progression.