Kennedy Institute of Rheumatology, Faculty of Medicine, Imperial College, London W6 8LH, UK.
Mediators Inflamm. 2010;2010:393946. doi: 10.1155/2010/393946. Epub 2010 Jun 24.
Inflammation drives atherosclerosis. Both immune and resident vascular cell types are involved in the development of atherosclerotic lesions. The phenotype and function of these cells are key in determining the development of lesions. Toll-like receptors are the most characterised innate immune receptors and are responsible for the recognition of exogenous conserved motifs on pathogens, and, potentially, some endogenous molecules. Both endogenous and exogenous TLR agonists may be present in atherosclerotic plaques. Engagement of toll-like receptors on immune and resident vascular cells can affect atherogenesis as signalling downstream of these receptors can elicit proinflammatory cytokine release, lipid uptake, and foam cell formation and activate cells of the adaptive immune system. In this paper, we will describe the expression of TLRs on immune and resident vascular cells, highlight the TLR ligands that may act through TLRs on these cells, and discuss the consequences of TLR activation in atherosclerosis.
炎症驱动动脉粥样硬化。免疫和固有血管细胞类型都参与了动脉粥样硬化病变的发展。这些细胞的表型和功能是决定病变发展的关键。 Toll 样受体是最具特征的先天免疫受体,负责识别病原体上的外源保守基序,以及潜在的一些内源性分子。在动脉粥样硬化斑块中可能存在内源性和外源性 TLR 激动剂。免疫和固有血管细胞上 Toll 样受体的激活会影响动脉粥样硬化的发生,因为这些受体的下游信号转导可以引起促炎细胞因子的释放、脂质摄取、泡沫细胞形成,并激活适应性免疫系统的细胞。在本文中,我们将描述 TLR 在免疫和固有血管细胞上的表达,强调可能通过这些细胞上的 TLR 发挥作用的 TLR 配体,并讨论 TLR 激活在动脉粥样硬化中的后果。