• G Bamias, K Stamatelopoulos, E Zampeli, A Protogerou, F Sigala, C Papamichael, P Christopoulos, G D Kitas, and P P Sfikakis.
• First Department of Propaedeutic and Internal Medicine, Laikon Hospital, Medical School, Ethnikon and Kapodistriakon Univesity, Athens, Greece.
• Clin. Immunol. 2013 May 1; 147 (2): 144-50.

AbstractInteractions 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 concentrations 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.Copyright © 2013 Elsevier Inc. All rights reserved.

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