CP-086 CD69 A>G (RS11052877) genetic polymorphism on the response to tocilizumab in rheumatoid arthritis patients

Abstract

BackgroundCD69 receptor is a C lectin transmembrane protein expressed by T cells, natural killer (NK) cells and active B cells. This receptor is involved in the production and regulation of T cells, B cells and NK cells, and these are involved in interleukin 6 (IL-6) production. IL-6 is a multifunctional glycoprotein involved in the immune response, inflammation and bone metabolism; IL-6 makes significant contributions to autoimmune and inflammatory diseases such as rheumatoid arthritis (RA). Tocilizumab is a humanised monoclonal antibody inhibitor of IL-6 receptor, indicated in combination with methotrexate in the treatment of RA in patients with inadequate response or intolerance to prior therapies.PurposeThe aim of this study was evaluate the role of the CD69 A>G (rs11052877) genetic polymorphism on the response to tocilizumab in RA patients.Material and methodsThe CD69 A>G (rs11052877) genetic polymorphism was genotyped using predesigned TaqMan genotyping assay technology and analysed on a ViiA7 real time PCR system. Clinical response was evaluated at 3, 6, 9 and 12 months after the first infusion of the drug, using the 28 joint disease activity score criteria (DAS28), and good responders were classified according to EULAR criteria. EULAR good response was defined as a change in DAS28 >1.2 and DAS28 ≤3.2. Statistical analysis was performed using SPSS V.20.ResultsClinical data from 140 tocilizumab treated patients were obtained. The patients were aged (mean±SD) 53.25±12.42 years and 79% were women. Even though we found a greater proportion of good responders among CD69 GG carriers than among A/G or A/A carriers at 3 months (60% vs 43.27%), 6 months (72.73% vs 59.17%), 9 months (76.19% vs 65.66%) and 12 months (90% vs 73.95%), these results were not statistically significant (p=0.17, p=0.22, p=0.34 and p=0.09)ConclusionThese results show that the CD69 A>G (rs11052877) genetic polymorphism by itself is not useful as a predictor of tocilizumab response in RA patients but its influence should be studied further.No conflict of interest

Toward Overcoming Treatment Failure in Rheumatoid Arthritis

“…Relationship between CD69 rs11052877 A alleles and good tocilizumab response was further validated in a study with 79 RA patients enrolled ( 300 ). In contrast, another study concluded that CD69 rs11052877 A/G genetic polymorphism was not useful as a predictor of tocilizumab response in RA patients ( 340 ). Data from 87 patients suggested that FCGR3A rs396991-TT could be used to predict better EULAR response ( 286 ).…”