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Journal of Lipid Research, Vol. 46, 829-838, May 2005
Copyright © 2005 by American Society for Biochemistry and Molecular Biology
Thematic Review |
Department of Pathology, University of Chicago, Chicago, IL 60637
1 To whom correspondence should be addressed. e-mail: reardon{at}uchicago.edu
Atherosclerosis is a complex inflammatory disease process involving an array of cell types and interactions. Although macrophage foam cells and vascular smooth muscle cells constitute the bulk of the atherosclerotic lesion, other cell types have been implicated in this disease process as well. These cellular components of both innate and adaptive immunity are involved in modulating the response of macrophage foam cells and vascular smooth muscle cells to the retained and modified lipids in the vessel wall as well as in driving the chronic vascular inflammation that characterizes this disease.
In this review, the involvement of a number of less prominent
leukocyte populations in the pathogenesis of atherosclerosis is discussed. More
specifically, the roles of natural killer cells, mast cells, neutrophils,
dendritic cells, 
T-cells, natural killer T-cells, regulatory T-cells,
and B-cells are addressed.
Abbreviations: apo,
apolipoprotein; 
-GalCer, -galactosylceramide; IL,
interleukin; LDLR–/–, low density lipoprotein
receptor-deficient; MCP-1, monocyte chemoattractant
protein-1; MHC, major histocompatibility complex; NK cell,
natural killer cell; NKT cell, natural killer T-cell; OxLDL,
oxidized low density lipoprotein; PAF, platelet-activating
factor; RAG, recombination-activating gene; TCR, T-cell
receptor; Th, T-helper; TNF, tumor necrosis
factor; Treg, regulatory T-cells
Supplementary key words innate and adaptive immunity • natural killer
cells • mast cells • neutrophils • dendritic
cells • T-cells • natural killer
T-cells • regulatory
T-cells • B-cells
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