期刊
ARTHRITIS RESEARCH & THERAPY
卷 17, 期 -, 页码 -出版社
BMC
DOI: 10.1186/s13075-015-0665-7
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资金
- European Community Innovative Medicines Initiative joint undertaking BeTheCure [115142]
- European Commission FP7 Health programme [FP7-HEALTH-F2-2012-305549]
- Landsteiner Foundation for Blood Transfusion Research [0912F]
- Dutch Arthritis Foundation
Introduction: Although the role of platelets in rheumatoid arthritis (RA) is relatively unexplored, recent studies point towards a contribution of platelets in arthritis. We set out to determine platelet phenotype in RA and studied whether this could be influenced by the presence of anti-citrullinated protein antibodies (ACPA). Methods: Platelets from healthy controls were incubated in the presence of plasma of patients with RA or age-and sex-matched healthy controls and plasma from ACPA(neg) or ACPA(pos) patients or in the presence of plate-bound ACPA. Characteristics of platelets isolated from patients with RA were correlated to disease activity. Results: Platelets isolated from healthy controls displayed markers of platelet activation in the presence of plasma derived from RA patients, as determined by P-selectin expression, formation of aggregates and secretion of soluble CD40 ligand (sCD40L). Furthermore, levels of P-selectin expression and sCD40L release correlated with high ACPA titres. In accordance with these findings, enhanced platelet activation was observed after incubation with ACPApos plasma versus ACPAneg plasma. Pre-incubation of platelets with blocking antibodies directed against low-affinity immunoglobulin G receptor (Fc gamma RIIa) completely inhibited the ACPA-mediated activation. In addition, expression of P-selectin measured as number of platelets correlated with Disease Activity Score in 44 joints, C-reactive protein level, ACPA status and ACPA level. Conclusions: We show for the first time that ACPA can mediate an Fc gamma RIIa-dependent activation of platelets. As ACPA can be detected several years before RA disease onset and activated platelets contribute to vascular permeability, these data implicate a possible role for ACPA-mediated activation of platelets in arthritis onset.
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