TY - JOUR T1 - Interleukin 10 and Tumor Necrosis Factor-α Genotypes in Rheumatoid Arthritis — Association with Clinical Response to Glucocorticoids JF - The Journal of Rheumatology JO - J Rheumatol SP - 503 LP - 511 DO - 10.3899/jrheum.090566 VL - 37 IS - 3 AU - BANESA de PAZ AU - MERCEDES ALPERI-LÓPEZ AU - FRANCISCO J. BALLINA-GARCÍA AU - CATUXA PRADO AU - LOURDES MOZO AU - CARMEN GUTIÉRREZ AU - ANA SUÁREZ Y1 - 2010/03/01 UR - http://www.jrheum.org/content/37/3/503.abstract N2 - Objective. There are dysregulated levels of interleukin 10 (IL-10) and tumor necrosis factor-α (TNF-α) in rheumatoid arthritis (RA), and their role in the disease is controversial. We analyzed the association of functional polymorphisms of IL-10 and TNF-α with susceptibility and disease characteristics at the time of diagnosis, and we also evaluated their possible use as predictors of clinical response to treatments. Methods. Patients with recent-onset RA (n = 162) and healthy controls (n = 373) were genotyped for −1082 IL-10 and −308 TNF-α polymorphisms and data were related to clinical and immunological measurements of patients at the time of diagnosis. Response to treatment after 6 months was determined in 125 patients by the absolute change in Disease Activity Score (DAS28) and the American College of Rheumatology criteria for improvement. Results. We found a reduced frequency of the low IL-10 producer genotype (−1082AA) in patients with RA compared to controls (26.5% vs 38.9%; p = 0.006), while it is a risk factor for anticyclic citrullinated peptide antibodies (anti-CCP) positivity (p = 0.028). Evaluation of clinical response to treatments indicated that carriage of the high IL-10 genotype was associated with a favorable outcome (p = 0.009), specifically to prednisone therapy (p = 0.0003). No significant effects were observed with TNF-α polymorphism alone; however, in combination with the IL-10 genotype, it increased the strength of these associations. Conclusion. Results show an association between the low IL-10 producer genotype and protection from RA; nevertheless, when other specific genetic and/or environmental factors trigger onset of RA, this genotype may predispose to development of anti-CCP+ RA disease with reduced response to prednisone treatment. ER -