Atherosclerosis: a chronic inflammatory disease mediated by mast cells.

Atherosclerosis: a chronic inflammatory disease mediated by mast cells.
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DOI:
10.5114/ceji.2015.54603
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发表时间:
2015
期刊:
Central-European journal of immunology
影响因子:
--
通讯作者:
Shaik-Dasthagirisaeb Y
Shaik-Dasthagirisaeb Y
中科院分区:
其他
文献类型:
--
作者:
Conti P;Shaik-Dasthagirisaeb Y

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炎症是动脉粥样硬化和免疫疾病发生发展的重要过程,涉及多种细胞类型,包括巨噬细胞、t淋巴细胞、内皮细胞、平滑肌细胞和肥大细胞。动脉粥样硬化的基本损害是动脉粥样硬化或纤维脂肪斑块,这是一种引起多种疾病的病变。在动脉粥样硬化中,巨噬细胞参与的先天免疫反应是由动脉内皮细胞发起的,动脉内皮细胞对修饰的脂蛋白作出反应,导致Th1细胞亚群活化,产生炎症细胞因子和趋化因子。其他免疫细胞,如在动脉粥样硬化的发生和发展中起关键作用的CD4+ T炎症细胞,以及对动脉粥样硬化的发展具有保护作用的调节性T细胞[Treg]也参与其中。大量证据表明肥大细胞及其产物在炎症和动脉粥样硬化中起关键作用。激活的肥大细胞可能会产生有害影响,引发基质降解、细胞凋亡、增强以及炎症细胞的募集,炎症细胞积极促进动脉粥样硬化和斑块的形成。本文讨论动脉粥样硬化、炎症和肥大细胞之间的关系。
Inflammation is a process that plays an important role in the initiation and progression of atherosclerosis and immune disease, involving multiple cell types, including macrophages, T-lymphocytes, endothelial cells, smooth muscle cells and mast cells. The fundamental damage of atherosclerosis is the atheromatous or fibro-fatty plaque which is a lesion that causes several diseases. In atherosclerosis the innate immune response, which involves macrophages, is initiated by the arterial endothelial cells which respond to modified lipoproteins and lead to Th1 cell subset activation and generation of inflammatory cytokines and chemoattractant chemokines. Other immune cells, such as CD4+ T inflammatory cells, which play a critical role in the development and progression of atherosclerosis, and regulatory T cells [Treg], which have a protective effect on the development of atherosclerosis are involved. Considerable evidence indicates that mast cells and their products play a key role in inflammation and atherosclerosis. Activated mast cells can have detrimental effects, provoking matrix degradation, apoptosis, and enhancement as well as recruitment of inflammatory cells, which actively contributes to atherosclerosis and plaque formation. Here we discuss the relationship between atherosclerosis, inflammation and mast cells.