Innate immunity and monocyte-macrophage activation in atherosclerosis

被引:99
作者
Shalhoub, Joseph [1 ,2 ]
Falck-Hansen, Mika A. [1 ]
Davies, Alun H. [2 ]
Monaco, Claudia [1 ]
机构
[1] Univ London Imperial Coll Sci Technol & Med, Fac Med, Kennedy Inst Rheumatol, London, England
[2] Univ London Imperial Coll Sci Technol & Med, Fac Med, Acad Sect Vasc Surg, Dept Surg & Canc, London, England
来源
JOURNAL OF INFLAMMATION-LONDON | 2011年 / 8卷
关键词
Atherosclerosis Inflammation; Innate immunity; Toll-like receptors; Monocyte subsets; Macrophage subtypes; Macrophage polarisation; TOLL-LIKE RECEPTOR-4; LOW-DENSITY-LIPOPROTEIN; OXIDIZED LOW-DENSITY; COLONY-STIMULATING FACTOR; CORONARY-ARTERY-DISEASE; BLOOD MONOCYTES; ALTERNATIVE ACTIVATION; LESION FORMATION; GENE-EXPRESSION; RHEUMATOID-ARTHRITIS;
D O I
10.1186/1476-9255-8-9
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Innate inflammation is a hallmark of both experimental and human atherosclerosis. The predominant innate immune cell in the atherosclerotic plaque is the monocyte-macrophage. The behaviour of this cell type within the plaque is heterogeneous and depends on the recruitment of diverse monocyte subsets. Furthermore, the plaque microenvironment offers polarisation and activation signals which impact on phenotype. Microenvironmental signals are sensed through pattern recognition receptors, including toll-like and NOD-like receptors - the latter of which are components of the inflammasome - thus dictating macrophage behaviour and outcome in atherosclerosis. Recently cholesterol crystals and modified lipoproteins have been recognised as able to directly engage these pattern recognition receptors. The convergent role of such pathways in terms of macrophage activation is discussed in this review.
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页数:17
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