RT Journal Article
SR Electronic
T1 Disease Activity Improvement in Rheumatoid Arthritis Treated with Tumor Necrosis Factor-α Inhibitors Correlates with Increased Soluble Fas Levels
JF The Journal of Rheumatology
JO J Rheumatol
FD The Journal of Rheumatology
SP 1961
OP 1965
DO 10.3899/jrheum.131544
VO 41
IS 10
A1 Romano, Eloisa
A1 Terenzi, Riccardo
A1 Manetti, Mirko
A1 Peruzzi, Francesca
A1 Fiori, Ginevra
A1 Nacci, Francesca
A1 Bellando-Randone, Silvia
A1 Matucci-Cerinic, Marco
A1 Guiducci, Serena
YR 2014
UL http://www.jrheum.org/content/41/10/1961.abstract
AB Objective. Rheumatoid arthritis (RA) is characterized by chronic synovial inflammation and hyperplasia. Tumor necrosis factor-α (TNF-α) plays a pivotal role in RA by interfering with the Fas–Fas ligand (FasL) proapoptotic pathway. We investigated the circulating levels of soluble Fas (sFas) and soluble FasL (sFasL), and their possible correlation with disease activity and improvement after anti-TNF-α treatment in RA. Methods. Serum levels of sFas and sFasL were measured by quantitative ELISA in 52 patients with RA before and after 3 months of anti-TNF-α treatment (adalimumab, n = 32; infliximab, n = 20). Disease activity measures [Disease Activity Score at 28 joints-erythrocyte sedimentation rate (DAS28-ESR), C-reactive protein (CRP)] were recorded before and after treatment. Forty age-matched and sex-matched healthy subjects served as controls. Results. No significant differences in serum sFas levels were detected between anti-TNF-α-naive patients with RA and controls. After anti-TNF-α treatment, serum sFas levels significantly increased in patients with RA compared to both anti-TNF-α-naive patients and controls. Increased sFas levels inversely correlated with disease activity variables (DAS28-ESR: r = −0.739, CRP: r = −0.636, both p < 0.001). No significant differences in sFasL levels were detected in patients with RA before and after anti-TNF-α treatment. Conclusion. In RA, an increase in sFas levels closely correlates with improvement in disease activity induced by TNF-α inhibitors, suggesting their ability to modulate Fas-mediated synoviocyte apoptosis.