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天然免疫、巨噬细胞活化与动脉粥样硬化。

Innate immunity, macrophage activation, and atherosclerosis.

作者信息

Yan Zhong-qun, Hansson Göran K

机构信息

Center for Molecular Medicine, Karolinska Institute, Stockholm, Sweden.

出版信息

Immunol Rev. 2007 Oct;219:187-203. doi: 10.1111/j.1600-065X.2007.00554.x.

Abstract

Inflammation underpins the development of atherosclerosis. Initiation and progression of vascular inflammation involves a complex cellular network, with macrophages as major contributors. Activated macrophages produce proinflammatory mediators, bridge innate and adaptive immunity, regulate lipid retention, and participate directly in vascular repair and remodeling. Recent efforts to elucidate molecular mechanisms involved in the regulation of vascular inflammation in atherosclerosis have implicated several families of innate immune recognition receptors in inflammatory activation during the course of this disease. This article reviews our current understanding of innate immune recognition receptors, signaling pathways, and putative ligands implicated in activation of macrophages in the disease. In its final section, we propose a model for the role of macrophages in bridging inflammation and atherosclerosis from the perspective of innate immune recognition and activation.

摘要

炎症是动脉粥样硬化发展的基础。血管炎症的起始和进展涉及一个复杂的细胞网络,其中巨噬细胞是主要贡献者。活化的巨噬细胞产生促炎介质,连接固有免疫和适应性免疫,调节脂质潴留,并直接参与血管修复和重塑。最近,为阐明动脉粥样硬化中血管炎症调节所涉及的分子机制,已有研究表明几个固有免疫识别受体家族在该疾病过程中的炎症激活中发挥作用。本文综述了我们目前对固有免疫识别受体、信号通路以及与该疾病中巨噬细胞激活相关的假定配体的理解。在最后一部分,我们从固有免疫识别和激活的角度提出了一个巨噬细胞在连接炎症和动脉粥样硬化中作用的模型。

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