Increased Th1 activity in patients with coronary artery disease

被引:82
作者
Fernandes, JL
Mamoni, RL
Orford, JL
Garcia, C
Selwyn, AP
Coelho, OR
Blotta, MHSL
机构
[1] Univ Sao Paulo, Inst Heart, Sch Med, BR-05403900 Sao Paulo, SP, Brazil
[2] Univ Estadual Campinas, UNICAMP, Campinas, SP, Brazil
[3] Brigham & Womens Hosp, Boston, MA 02115 USA
基金
巴西圣保罗研究基金会;
关键词
atherosclerosis; coronary artery disease; inflammation; interleukins;
D O I
10.1016/j.cyto.2004.01.007
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Background: Atherosclerotic lesions Lire mainly composed of macrophages and T lymphocytes. Specific T helper type I (Th1) cytokines and interferon gamma (IFN-gamma) inducible chemokines have been shown to be present in these lesions, modulating the local immunologic response. To explore whether this increase in Th1 activity could also be detected in circulating cells indicating a systemic activation, we studied the peripheral expression of Th I cytokines and chemokines in patients with coronary artery disease and controls. Methods and results: Fifty patients with coronary artery disease (25 with unstable angina and 25 with stable angina) and 10 controls were studied. Serum interleukin (IL)-12 and IFN-gamma and the expression of IFN-gamma inducible chemokines IP-10, Mig and their receptor CXCR3 in peripheral cells were analyzed. Serum IL-12 and intracellular expression of IFN-gamma were significantly elevated in patients with unstable angina. An enhanced expression of IFN-gamma chemokines IP-10, Mig and CXCR3 in patients with stable angina was also observed. Conclusions: This study demonstrates an increased systemic inflammatory activity in patients with coronary heart disease with a predominant Th1 response, particularly in patients with unstable angina, suggesting an important role played by this polarization in plaque formation and rupture. (C) 2004 Elsevier Ltd. All rights reserved.
引用
收藏
页码:131 / 137
页数:7
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