Type I interferon-related genes in peripheral blood of patients with early rheumatoid arthritis and its association with disease activity

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Background and objectives. Rheumatoid arthritis (RA) is a progressive systemic autoimmune disorder that mainly targets the joints, causing inflammation and destruction of affected joints. The main therapeutic goal is to prevent joint destruction, preserve function, and maintain a better quality of life. The type I interferon (IFN-I) signature, characterized by increased expression of interferon-response genes, is present in a subset of RA patients and may serve as a potential biomarker for disease activity and prognosis. The purpose of this study was to shed light on the role of the IFN-I signature in patients with RA. Materials and methods. The study included 100 participants: 50 RA patients and 50 healthy controls. History taking, clinical assessment, and disease activity scoring were performed in all patients, along with anti-cyclic citrullinated peptide (anti-CCP) and rheumatoid factor (RF) measurements. Whole blood samples were obtained, and quantitative real-time polymerase chain reaction (qPCR) was performed to assess the mRNA expression levels of IFI44L, IFNAR1, and IFNAR2. Results. IFI44L, IFNAR1, and IFNAR2 were significantly upregulated in RA patients and showed significant positive correlations with DAS28, anti-CCP, and RF (all p < 0.001). The strongest correlation was observed between IFI44L and anti-CCP (r = 0.671). ROC analysis showed high discriminatory performance within the studied cohort, with AUC values of 0.974 for IFI44L, 0.982 for IFNAR1, and 0.984 for IFNAR2. Conclusions. Patients with RA showed a high IFN-I signature, supporting its role in disease pathogenesis and activity.

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