Brigham and Women's Hospital, Harvard Medical School, 77 Avenue Louis Pasteur, NRB7, Boston, MA 02115, USA.
Immunity. 2013 Jun 27;38(6):1092-104. doi: 10.1016/j.immuni.2013.06.009.
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.
根据传统观点，动脉粥样硬化是由于胆固醇在动脉壁中被动积聚而导致的。然而，不断涌现的证据表明炎症和免疫效应机制在这种疾病的发病机制中起作用。先天免疫和适应性免疫在动脉粥样硬化形成过程中起作用，并将许多传统危险因素与动脉功能改变联系起来。炎症途径已成为寻求针对心血管疾病的新型预防和治疗策略的靶点，心血管疾病是全世界发病率和死亡率不断上升的主要原因。在这里，我们通过免疫学的视角回顾动脉粥样硬化发病机制的当前实验和临床知识，以及对物种生存至关重要的宿主防御机制如何实际上导致这种慢性疾病，但也为其缓解提供了新的机会。
