摘要
动脉粥样硬化,心血管疾病(CVD)的主要危险因素,全球死亡的主要原因,是一个多因子的慢性炎性疾病。其中,临床表现始于早期动脉壁上富含脂质病灶斑块破裂和/或血栓形成。髓细胞室,包括巨噬细胞和树突状细胞(树突状细胞),是众所周知的引起动脉粥样硬化的发生和发展。然而他们复杂的表型异质性阻碍了我们充分认识他们的角色。在这里,我们综述了动脉粥样硬化中髓系细胞的生物学特性和功能多样性。几个不同的细胞亚群的巨噬细胞和髓样细胞已经确定在动脉粥样硬化斑块,包括特定的动脉粥样硬化本身的亚群。我们的能力对于他们的治疗目标是有限的。未来的挑战是在治疗方法,旨在针对特定的髓细胞亚群防止动脉粥样硬化的髓系细胞亚群激活的同时保留抗动脉粥样硬化的髓系细胞的修复功能。
关键词: 适应性免疫,动脉粥样硬化,树突细胞,炎症,先天免疫,巨噬细胞,髓系
图形摘要
Current Drug Targets
Title:Macrophages and Dendritic Cells: The Usual Suspects in Atherogenesis
Volume: 16 Issue: 4
Author(s): Christina Kassiteridi and Claudia Monaco
Affiliation:
关键词: 适应性免疫,动脉粥样硬化,树突细胞,炎症,先天免疫,巨噬细胞,髓系
摘要: Atherosclerosis, the major risk factor for cardiovascular disease (CVD) and the leading cause of death worldwide, is a multifactorial chronic inflammatory disease, which, clinically manifests from early lipid-rich lesions to plaque rupture and/or thrombosis in the arterial wall. The myeloid cell compartment, including macrophages and dendritic cells (DCs), is long known to contribute to the initiation and progression of atherosclerosis. However their complex phenotypic heterogeneity hampers our full understanding of their role. Here, we review the biological and functional versatility of the myeloid cells in atherosclerosis. Several distinct subsets of macrophages and myeloid cells have been identified in atherosclerotic plaques, including subsets that are specific to atherosclerosis itself. Our ability to target them therapeutically is still limited. The challenge for the future will be the definition of treatments that target specific myeloid subsets to prevent the activation of pro-atherogenic myeloid cell subsets while preserving the anti-atherogenic and repairable function of myeloid cells.
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Cite this article as:
Christina Kassiteridi and Claudia Monaco , Macrophages and Dendritic Cells: The Usual Suspects in Atherogenesis, Current Drug Targets 2015; 16 (4) . https://dx.doi.org/10.2174/1389450116666150330115809
DOI https://dx.doi.org/10.2174/1389450116666150330115809 |
Print ISSN 1389-4501 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5592 |
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