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首页> 外文期刊>Current opinion in lipidology >Oxidized low density lipoprotein and innate immune receptors.
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Oxidized low density lipoprotein and innate immune receptors.

机译：氧化的低密度脂蛋白和先天免疫受体。

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SUMMARY: PURPOSE OF REVIEW Atherosclerosis is now recognized as a chronic inflammatory disease. This review discusses recent literature reporting that innate immune receptors bind oxidatively modified LDL and its many oxidized moieties and consequently modulate the atherogenic process. These innate pattern recognition receptors are known to play a central role in pro-inflammatory responses to bacteria by binding pathogen-associated molecular patterns. It is hypothesized that oxidized LDL exposes similar molecular patterns recognized by receptors of innate immunity.RECENT FINDINGS Minimally modified LDL and its oxidized phospholipids have been found to bind to CD14 or activate Toll-like receptors on macrophages. In turn, various biological activities have been induced, including the stimulation of cytoskeletal rearrangements that alter phagocytic activity and the stimulation of cytokine secretion, such as IL-8. These findings link modified LDL with innate pattern recognition receptors, such as those involved in the lipopolysaccharide signaling pathway. Human epidemiological studies support the involvement of CD14 and TLR4 in cardiovascular diseases. Oxidized LDL has also been demonstrated to bind to C-reactive protein, an opsonic molecule activating classic complement pathway and Fcgamma receptor endocytosis. These data suggest that C-reactive protein may not only be a strong predictor of clinical disease, but may also play a role in atherogenesis. Recent data on other innate immune receptors are discussed in the context of their potential interactions with oxidized LDL and atherogenesis.SUMMARY Recent findings suggest that oxidized forms of LDL interact with innate immune receptors. Further studies are needed to identify the role of these interactions in inflammation and atherosclerosis.
机译：概述：审查的目的动脉粥样硬化现已被认为是一种慢性炎症性疾病。这篇综述讨论了最近的文献报道，即先天免疫受体结合氧化修饰的LDL及其许多氧化部分，从而调节动脉粥样硬化过程。已知这些先天性模式识别受体通过结合病原体相关的分子模式，在对细菌的促炎反应中发挥重要作用。据推测，氧化的LDL会暴露出先天免疫受体所识别的相似分子模式。最新发现已发现最小修饰的LDL及其氧化的磷脂与CD14结合或激活巨噬细胞上的Toll样受体。反过来，已经诱导了各种生物学活性，包括刺激改变吞噬活性的细胞骨架重排和刺激细胞因子分泌，例如IL-8。这些发现将修饰的LDL与固有的模式识别受体联系起来，例如与脂多糖信号传导途径有关的受体。人类流行病学研究支持CD14和TLR4参与心血管疾病。氧化的LDL还被证明与C反应蛋白结合，后者是激活经典补体途径和Fcγ受体胞吞作用的调理素分子。这些数据表明，C反应蛋白不仅可能是临床疾病的有力预测指标，而且还可能在动脉粥样硬化中发挥作用。在其他先天免疫受体与氧化的LDL和动脉粥样硬化潜在相互作用的背景下讨论了最新数据。总结最新发现表明，氧化形式的LDL与先天免疫受体相互作用。需要进一步的研究来确定这些相互作用在炎症和动脉粥样硬化中的作用。

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