Immune Effector Mechanisms Implicated in Atherosclerosis: From Mice to Humans

被引:540
作者
Libby, Peter [1 ]
Lichtman, Andrew H. [1 ]
Hansson, Goran K. [2 ,3 ]
机构
[1] Harvard Univ, Sch Med, Brigham & Womens Hosp, Boston, MA 02115 USA
[2] Karolinska Univ Hosp, Karolinska Inst, Dept Med, S-17176 Stockholm, Sweden
[3] Karolinska Univ Hosp, Karolinska Inst, Ctr Mol Med, S-17176 Stockholm, Sweden
基金
美国国家卫生研究院; 瑞典研究理事会;
关键词
LOW-DENSITY-LIPOPROTEIN; SMOOTH-MUSCLE-CELLS; ACUTE CORONARY SYNDROME; REGULATORY T-CELLS; HEAT-SHOCK PROTEIN-65; C-REACTIVE PROTEIN; PROMOTES EARLY ATHEROSCLEROSIS; RECEPTOR-DEFICIENT MICE; REDUCES ATHEROSCLEROSIS; INTERFERON-GAMMA;
D O I
10.1016/j.immuni.2013.06.009
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
According to the traditional view, atherosclerosis results from a passive buildup of cholesterol in the artery wall. Yet, burgeoning evidence implicates inflammation and immune effector mechanisms in the pathogenesis of this disease. Both innate and adaptive immunity operate during atherogenesis and link many traditional risk factors to altered arterial functions. Inflammatory pathways have become targets in the quest for novel preventive and therapeutic strategies against cardiovascular disease, a growing contributor to morbidity and mortality worldwide. Here we review current experimental and clinical knowledge of the pathogenesis of atherosclerosis through an immunological lens and how host defense mechanisms essential for survival of the species actually contribute to this chronic disease but also present new opportunities for its mitigation.
引用
收藏
页码:1092 / 1104
页数:13
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