Kennedy Institute of Rheumatology, Faculty of Medicine, Imperial College, London, United Kingdom.
Clin Chim Acta. 2012 Jan 18;413(1-2):3-14. doi: 10.1016/j.cca.2011.08.021. Epub 2011 Aug 22.
Atherosclerosis is a multi-factorial inflammatory disease and is the primary initiator of coronary artery and cerebrovascular disease. Initially believed to be exclusively lipid-driven, recent evidence demonstrates that inflammation is a significant driving force of the disease. Cellular components of innate immunity, for example monocytes and macrophages, play a predominant role in atherosclerosis. Toll-like receptors (TLRs) are the most characterised innate immune receptors and recent evidence demonstrates an important role in atherogenesis. Engagement of TLRs results in the transcription of pro-inflammatory cytokines, foam cell formation and activation of adaptive immunity. Recently they have also been implicated in protection from vascular disease. In this review, we detail the role of the innate immune system, specifically macrophages and TLR signalling, in atherosclerosis and acute cardiovascular complications, and thereby identify the potential of TLRs to act as therapeutic targets.
动脉粥样硬化是一种多因素炎症性疾病,是冠状动脉和脑血管疾病的主要启动因素。最初认为它是纯粹的脂质驱动的疾病,但最近的证据表明炎症是该疾病的一个重要驱动因素。先天免疫的细胞成分,如单核细胞和巨噬细胞,在动脉粥样硬化中起着主要作用。Toll 样受体 (TLRs) 是最具特征的先天免疫受体,最近的证据表明它们在动脉粥样硬化形成中具有重要作用。TLRs 的激活导致促炎细胞因子的转录、泡沫细胞形成和适应性免疫的激活。最近,它们也被认为可以预防血管疾病。在这篇综述中,我们详细描述了先天免疫系统,特别是巨噬细胞和 TLR 信号在动脉粥样硬化和急性心血管并发症中的作用,并由此确定了 TLR 作为治疗靶点的潜力。