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冠心病患者亚组中T细胞增殖和白细胞介素-2产生缺陷

Defective T-cell Proliferation and IL-2 Production in a Subgroup of Patients with Coronary Artery Disease.

作者信息

Mahmoudi Maryam, Siassi Fereydoon, Mahmoudi Mohammad Jafar, Eshraghian Mohammad Reza, Zarnani Amir Hassan, Rezaei Nima, Hedayat Mona, Shokri Fazel, Saboor-Yaraghi Ali-Akbar

机构信息

Department of Nutrition and Biochemistry, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran.

出版信息

Iran J Allergy Asthma Immunol. 2010 Sep;9(3):133-40.

PMID:20952802
Abstract

Atherosclerosis is a chronic inflammatory disease of the arterial wall characterized by innate and adaptive immune responses to a variety of microbial and self-antigens. Given the crucial role of adaptive immunity in the pathogenesis of atherosclerosis, this study was performed to investigate the proliferative response of peripheral blood mononuclear cells (PBMC) and interleukin (IL)-2 production in patients with coronary artery disease (CAD). In this study, 25 patients with chronic stable CAD and 25 healthy individuals were investigated. The PBMCs were separated and stimulated with phytohaemagglutinin (PHA). MTT assay was performed to measure cell viability and proliferation. IL-2 concentrations in cell culture supernatants were determined by Enzyme-Linked Immunosorbent Assay. PHA-stimulated cells revealed a significantly increased optical density (OD) in both groups of patients (p=0.004) and controls (p<0.001). However, the patient group showed a significantly lower Stimulation index (SI) (p=0.001). Upon in vitro stimulation with PHA, IL-2 levels were significantly increased in both groups of patients and controls (p<0.001). However, IL-2 concentrations were significantly lower in the patient group (p=0.018). Six patients showed defective IL-2 production, whereas similar finding was not observed in the normal control subjects (p=0.022). PBMCs from patients with coronary artery disease showed defective PHA-induced mitogenesis and IL-2 production. Considering the autoimmune nature of atherosclerosis, decreased IL-2 production may potentially enhance the atherogenic process, leading to spontaneous activation of autoreactive T lymphocytes.

摘要

动脉粥样硬化是一种动脉壁的慢性炎症性疾病,其特征是对多种微生物和自身抗原产生先天性和适应性免疫反应。鉴于适应性免疫在动脉粥样硬化发病机制中的关键作用,本研究旨在调查冠心病(CAD)患者外周血单个核细胞(PBMC)的增殖反应和白细胞介素(IL)-2的产生。在本研究中,对25例慢性稳定型CAD患者和25名健康个体进行了调查。分离PBMC并用植物血凝素(PHA)刺激。采用MTT法检测细胞活力和增殖情况。通过酶联免疫吸附测定法测定细胞培养上清液中的IL-2浓度。PHA刺激的细胞在患者组(p = 0.004)和对照组(p < 0.001)中均显示光密度(OD)显著增加。然而,患者组的刺激指数(SI)显著较低(p = 0.001)。在用PHA进行体外刺激后,患者组和对照组的IL-2水平均显著升高(p < 0.001)。然而,患者组的IL-2浓度显著较低(p = 0.018)。6例患者表现出IL-2产生缺陷,而正常对照组未观察到类似结果(p = 0.022)。冠心病患者的PBMC显示PHA诱导的有丝分裂和IL-2产生存在缺陷。考虑到动脉粥样硬化的自身免疫性质,IL-2产生减少可能会潜在地增强动脉粥样硬化进程,导致自身反应性T淋巴细胞的自发激活。

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