Circulating levels of TNF-like cytokine 1A correlate with the progression of atheromatous lesions in patients with rheumatoid arthritis G. Bamias a , 1 , K. Stamatelopoulos b , 1 , E. Zampeli a , A. Protogerou a , F. Sigala c , C. Papamichael b , P. Christopoulos a , G.D. Kitas a , P.P. Sfikakis a , ⁎ a First Department of Propaedeutic and Internal Medicine, Laikon Hospital, Medical School, Ethnikon and Kapodistriakon Univesity, Athens, Greece b Vascular Laboratory, Department of Clinical Therapeutics, Alexandra Hospital, Medical School, Ethnikon and Kapodistriakon Univesity, Athens, Greece c First Department of Propaedeutic Surgery, Hippocrateion Hospital, Medical School, Ethnikon and Kapodistriakon Univesity, Athens, Greece Received 19 December 2012; accepted with revision 1 March 2013 Available online 26 March 2013 KEYWORDS TNF-like cytokine 1A (TL1A); Death receptor 3 (DR3); Decoy receptor 3 (DcR3); Rheumatoid arthritis; Atherogenesis Abstract Interactions between TNF-like Cytokine 1A (TL1A) and its receptors, death receptor-3 (DR3) and decoy receptor-3 (DcR3) may be important in atherogenesis. We hypothesized that dysregulation of this system predicts formation of new atheromatic plaques in rheumatoid arthritis (RA). Forty-five patients were prospectively followed up for 40.5 ± 3.6 months. Serum concentra- tions of TL1A and DcR3 were measured at baseline and carotid and femoral arteries examined by ultrasound at baseline and at the end of follow-up. Individual serum levels of TL1A correlated with the progression of carotid atheromatic plaque height (Spearman rho = 0.550, p = 0.003). Patients with low TL1A and undetectable DcR3 serum levels at baseline showed significantly fewer newly formed carotid plaques during the next 3.5 years than the remaining patients (P = 0.016). Univariate analysis showed that a “low TL1A/DcR3” immunophenotype predicted a preserved atherosclerosis profile in carotid (P = 0.026), or carotid and/or femoral arteries (P = 0.022). Dysregulated TL1A- induced signaling may be associated with risk for accelerated atherosclerosis in RA. © 2013 Elsevier Inc. All rights reserved. 1. Introduction In recent years, it has been increasingly recognized that patients with RA are at elevated risk for cardiovascular (CV) disease [1]. The etiology of this association has not been fully elucidated yet. Nevertheless, current evidence supports a central pathogenetic role for the dysgerulated immune ⁎ Corresponding author at: 1st Department of Propeudetic and Internal Medicine, Medical School, Ethnikon and Kapodistriakon Univesity, Athens, Greece, 18 Ipsilantou Street, 10676 Athens, Greece. E-mail address: psfikakis@med.uoa.gr (P.P. Sfikakis). 1 The first 2 authors contributed equally to the present work. 1521-6616/$ - see front matter © 2013 Elsevier Inc. All rights reserved. http://dx.doi.org/10.1016/j.clim.2013.03.002 available at www.sciencedirect.com Clinical Immunology www.elsevier.com/locate/yclim Clinical Immunology (2013) 147, 144–150