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首页> 外文期刊>Current opinion in lipidology >Multiple roles of Toll-like receptor signaling in atherosclerosis.
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Multiple roles of Toll-like receptor signaling in atherosclerosis.

机译：Toll样受体信号转导在动脉粥样硬化中的多重作用。

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PURPOSE OF REVIEW: Toll-like receptors are key regulators of both innate and adaptive immune responses. This review outlines the recently emerged multiple roles of Toll-like receptor signaling in atherosclerosis. RECENT FINDINGS: Mice deficient in TLR4, TLR2 and MyD88 all have reduced atherosclerosis which establishes that Toll-like receptor-dependent pathways contribute to disease development. Although it is likely that total "infectious burden" contributes to atherosclerosis progression, endogenous ligands may also initiate and modulate Toll-like receptor signaling pathways. CD36, with established roles in recognition of endogenous ligands and atherosclerotic disease, facilitates TLR2 signaling and might therefore represent a bridge between endogenous lipid ligands and Toll-like receptor pathways. Furthermore, lipoprotein oxidation generates ligands that activate Toll-like receptor pathways. At the same time, Toll-like receptor activation may be inhibited by accumulating oxidized phospholipids, whichcould result in reduced dendritic cell maturation and impaired immunological priming. SUMMARY: Activation of Toll-like receptor signaling can promote atherosclerosis by multiple mechanisms, while some beneficial Toll-like receptor pathways may be inhibited by lipid accumulation. Due to their central role in the disease process, Toll-like receptor signaling pathways represent a target of immunomodulatory therapy with the goal of tipping the balance from excessive chronic inflammation towards resolution of inflammation, while not compromising host defense or atheroprotective immune functions.
机译：审查目的：Toll样受体是先天和适应性免疫反应的关键调节剂。这篇综述概述了Toll样受体信号在动脉粥样硬化中最近出现的多种作用。最近的发现：缺乏TLR4，TLR2和MyD88的小鼠均具有减少的动脉粥样硬化，这表明Toll样受体依赖性途径有助于疾病的发展。尽管总的“传染性负担”可能有助于动脉粥样硬化的进展，但内源性配体也可能启动和调节Toll样受体信号通路。具有识别内源性配体和动脉粥样硬化疾病作用的CD36促进TLR2信号传导，因此可能代表内源性脂质配体和Toll样受体途径之间的桥梁。此外，脂蛋白氧化产生可激活Toll样受体途径的配体。同时，Toll样受体的活化可能会通过积累氧化磷脂而受到抑制，这可能导致树突状细胞成熟度降低和免疫学引发受损。摘要：Toll样受体信号的激活可以通过多种机制促进动脉粥样硬化，而一些有益的Toll样受体途径可能被脂质蓄积所抑制。由于其在疾病过程中的重要作用，Toll样受体信号通路代表了免疫调节疗法的目标，其目标是使平衡从过度的慢性炎症转向炎症的消退，同时又不损害宿主防御或抗动脉粥样硬化的免疫功能。

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