Background Rheumatoid arthritis (RA) is a common immflamatory autoimmune disease characterized by persistent synovitis and progressive destruction of cartilage and bone in multiple joints. Among the autoantibodies detected in RA patients, circulating autoantibodies, anti-citrullinated protein/peptide antibodies (ACPA), are highly specific and useful diagnostic tools for RA. ACPA production seems to depend on antigen-specific CD4 (+) helper T cell activation. Activation of T cells requires costimulatory signals via binding of CD28 receptor with CD80/CD86 located on antigen-presenting cells (APC). Abatacept (ABA) is a biological agent for RA treatment, consisting of extracellular domains from cytotoxic T-lymphocyte antigen-4 and the Fc portion of human immunoglobulin G1 (CTLA-4-Ig) which competes with CD28 for CD80/86 binding.

Objectives This study aims to clarify how 48-week ABA treatment affects CD4 (+) T cell activation and ACPA production in RA patients.

Methods Peripheral blood mononucleated cells (PBMCs) and plasma were obtained from 30 patients enrolled in abatacept research outcome as a first-line biological agent in the real world (ABROAD study) at baseline, 24 and 48 weeks of ABA treatment. Fifty-three healthy individuals (HIs) were also enrolled as controls. Surface phenotypes and activation markers of T cells were analyzed with flow cytometory. ACPA titers were measured with EliA CCP ELISA kit.

Results Twenty-five patients (83.3%) were ACPA (+) (>4.5 U/mL). DAS28-CRP and SDAI were significantly reduced at 24 and 48 weeks compared with those at baseline. The proportion of CD25 (+) in CD4 (+) T cells in ACPA (+) group was significantly higher than those of ACPA (-) group and HIs at baseline (13.9±5.4% in ACPA (+) group; 6.7±2.9% in ACPA (-) group, p=0.0089; 7.1±4.6% in HIs, p<0.0001). The proportion of CD25 (+) in CD4 (+) T cells decreased at 24 and 48 weeks (13.9±5.4% at baseline; 6.6±5.8% at 24 weeks, p<0.0001; 6.1±3.1% at 48 weeks, p<0.0001). However, ACPA titers were not significantly changed at 24 and 48 weeks compared with those at baseline.

Conclusions 48-week T cell co-stimulation blockade reduces disease activities and the proportion of CD25 (+) in CD4 (+) T cells but not the ACPA titers in ACPA (+) RA patients.

Disclosure of Interest M. Murakami Speakers bureau: Bristol-Myers Squibb Japan, M. Ito: None declared, M. Sekiguchi Grant/research support: Bristol-Myers Squibb Japan, Speakers bureau: Bristol-Myers Squibb Japan, K. Matsui Grant/research support: Bristol-Myers Squibb Japan, M. Kitano Grant/research support: Bristol-Myers Squibb Japan, Y. Imura Grant/research support: Bristol-Myers Squibb Japan, K. Ohmura Grant/research support: Bristol-Myers Squibb Japan, T. Fujii Grant/research support: Bristol-Myers Squibb Japan, T. Kuroiwa: None declared, K. Maeda: None declared, S. Morita: None declared, Y. Kawahito Grant/research support: Bristol-Myers Squibb Japan, T. Mimori Grant/research support: Bristol-Myers Squibb Japan, H. Sano Grant/research support: Bristol-Myers Squibb Japan, N. Nishimoto Grant/research support: Bristol-Myers Squibb Japan

DOI 10.1136/annrheumdis-2014-eular.3997