Circulating levels of TNF-like cytokine 1A correlate with the progression of atheromatous lesions in patients with rheumatoid arthritis
Circulating levels of TNF-like cytokine 1A correlate with the progression of atheromatous lesions in patients with rheumatoid arthritis
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DOI：
10.1016/j.clim.2013.03.002
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发表时间：
2013-05-01
影响因子：
8.6
通讯作者：
Sfikakis, P. P.
中科院分区：
文献类型：
--
作者：
Bamias, G.;Stamatelopoulos, K.;Sfikakis, P. P.
肿瘤坏死因子样细胞因子1A（TL 1A）及其受体死亡受体3（DR 3）和诱骗受体3（DcR 3）之间的相互作用可能在动脉粥样硬化的发生中起重要作用。我们假设，该系统的失调预示着类风湿性关节炎（RA）中新的动脉粥样斑块的形成。45例患者前瞻性随访40.5 ± 3.6个月。在基线时测量血清TL 1A和DcR 3浓度，并在基线和随访结束时通过超声检查颈动脉和股动脉。TL 1A的个体血清水平与颈动脉粥样硬化斑块高度的进展相关（斯皮尔曼rho = 0.550，p = 0.003）。基线时TL 1A水平较低且DcR 3血清水平检测不到的患者在接下来的3.5年中显示出比其余患者显著更少的新形成的颈动脉斑块（P = 0.016）。单变量分析显示，“低TL 1A/DcR 3”免疫表型预测颈动脉（P = 0.026）或颈动脉和/或股动脉（P = 0.022）中保留的动脉粥样硬化特征。TL 1A诱导的信号转导失调可能与RA中动脉粥样硬化加速的风险相关(C)2013 Elsevier Inc. All rights reserved.
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 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. (C) 2013 Elsevier Inc. All rights reserved.