Center for Molecular Medicine, L8:03, Department of Medicine, Karolinska Institute, Stockholm SE-17176, Sweden.
Clin Immunol. 2010 Jan;134(1):5-24. doi: 10.1016/j.clim.2009.07.016. Epub 2009 Sep 9.
Atherosclerosis is a chronic disease characterised by lipid retention and inflammation in the arterial intima. Innate immune mechanisms are central to atherogenesis, involving activation of pattern-recognition receptors (PRRs) and induction of inflammatory processes. In a complex tissue, such as the atherosclerotic lesion, innate signals can originate from several sources and promote atherogenesis through ligation of PRRs. The receptors recognise conserved molecular patterns on pathogens and endogenous products of tissue injury and inflammation. Activation of PRRs might affect several aspects of atherosclerosis by acting on lesion resident cells. Scavenger receptors mediate antigen uptake and clearance of lipoproteins, thereby promoting foam cell formation. Signalling receptors, such as Toll-like receptors (TLRs), lead to induction of pro-inflammatory cytokines and antigen-specific immune responses. In this review we describe the innate mechanisms present in the plaque. We focus on TLRs, their cross-talk with other PRRs, and how their signalling cascades influence inflammation within the atherosclerotic lesion.
动脉粥样硬化是一种以动脉内膜脂质蓄积和炎症为特征的慢性疾病。先天免疫机制是动脉粥样硬化形成的核心，涉及模式识别受体（PRRs）的激活和炎症过程的诱导。在动脉粥样硬化病变等复杂组织中，先天信号可以来自多个来源，并通过 PRRs 的配体结合促进动脉粥样硬化形成。这些受体识别病原体和组织损伤及炎症的内源性产物上的保守分子模式。PRRs 的激活可能通过作用于病变部位的固有细胞，影响动脉粥样硬化的多个方面。清道夫受体介导抗原摄取和脂蛋白清除，从而促进泡沫细胞形成。信号受体，如 Toll 样受体（TLRs），导致促炎细胞因子和抗原特异性免疫反应的诱导。在这篇综述中，我们描述了斑块中的先天机制。我们重点介绍 TLRs、它们与其他 PRRs 的相互作用，以及它们的信号级联如何影响动脉粥样硬化病变中的炎症。
