RT Journal Article SR Electronic T1 Cytokines and Regulatory T Cells in Rheumatoid Arthritis and Their Relationship with Response to Corticosteroids JF The Journal of Rheumatology JO J Rheumatol FD The Journal of Rheumatology SP 2502 OP 2510 DO 10.3899/jrheum.100324 VO 37 IS 12 A1 BANESA de PAZ A1 MERCEDES ALPERI-LÓPEZ A1 FRANCISCO J. BALLINA-GARCÍA A1 CATUXA PRADO A1 CARMEN GUTIÉRREZ A1 ANA SUÁREZ YR 2010 UL http://www.jrheum.org/content/37/12/2502.abstract AB Objective. To analyze circulating cytokines and regulatory T cells (Treg) in patients with rheumatoid arthritis (RA) of different durations, and their association with functional interleukin 10 (IL-10) and tumor necrosis factor-α (TNF-α) genotypes in patients treated with corticosteroids. Methods. Serum levels of IL-6, IL-10, IL-17, IL-18, TNF-α, and transforming growth factor-ß (TGF-ß) were quantified in 196 patients and 61 healthy controls. Percentage of CD4+CD25high cells was determined by flow cytometry and Foxp3 expression by real-time reverse-transcription polymerase chain reaction. Data were related to clinical measurements and presence of the genotype −1082GG IL-10/−308GG TNF-α, previously associated with good response to corticosteroids. Results. Levels of TNF-α, IL-6, and IL-18 were significantly higher in patients compared to controls, while TGF-ß and IL-10 were lower. Serum samples of patients at disease onset (n = 32) had increased IL-6 and decreased TGF-ß, but there were no differences in other cytokines. These patients also presented a higher percentage of CD4+CD25high cells than those with established disease, although no significant differences were detected in Foxp3. Patients under corticosteroid treatment who were carriers of the good responder genotype had higher levels of TGF-ß, Foxp3, and Treg compared to patients with other genotypes, while relatively lower levels of TNF-α and IL-17 were observed. Conclusion. Patients at onset of RA present fewer alterations in cytokine levels and Treg than those with longer disease duration, supporting the role of disease progression in subsequent changes. The antiinflammatory balance observed in high IL-10/low TNF-α patients treated with prednisone supports the use of these genetic polymorphisms as predictors of response to corticosteroid therapy.