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Review
. 2013 Oct;24(5):371-80.
doi: 10.1097/MOL.0b013e328363d298.

Myeloid cells in atherosclerosis: a delicate balance of anti-inflammatory and proinflammatory mechanisms

Ekaterina K Koltsova  1 , Catherine C Hedrick, Klaus Ley
Affiliations
Review

Myeloid cells in atherosclerosis: a delicate balance of anti-inflammatory and proinflammatory mechanisms

Ekaterina K Koltsova et al. Curr Opin Lipidol. 2013 Oct.

Abstract

Purpose of review: Atherosclerosis is chronic disease, whose progression is orchestrated by the balance between proinflammatory and anti-inflammatory mechanisms. Various myeloid cells, including monocytes, macrophages, dendritic cells and neutrophils can be found in normal and atherosclerotic aortas, in which they regulate inflammation and progression of atherosclerosis. The lineage relationship between blood monocyte subsets and the various phenotypes and functions of myeloid cells in diseased aortas is under active investigation.

Recent findings: Various subsets of myeloid cells play diverse roles in atherosclerosis. This review discusses new findings in phenotypic and functional characterization of different subsets of macrophages, in part determined by the transcription factors IRF5 and Trib1, and dendritic cells, characterized by the transcription factor Zbtb46, in atherosclerosis.

Summary: Improved understanding proinflammatory and anti-inflammatory mechanisms of macrophages and dendritic cell functions is needed for better preventive and therapeutic measures in atherosclerosis.

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Conflict of interest statement

Conflicts of interest

There are no conflicts of interest.

Figures

FIGURE 1
FIGURE 1
Myeloid cells in atherosclerosis development. (a) The normal aorta contains some T lymphocytes and a small number of myeloid cells that express M2 markers and may be resident vascular macrophages. (b) Early atherosclerotic lesions are characterized by accumulation of myeloid cells in the subendothelial space. The number of cells in the adventitia is significantly increased. The macrophage population now represents a mixture of ‘M1-like’ and ‘M2-like’ macrophages. Various types of dendritic cells (DC) start to accumulate in both adventitia and plaque. (c) Late atherosclerotic lesions are characterized by accumulation of cholesterol crystals and various types of immune cells including foam cells, whose death leads to formation of the necrotic core, which is related to plaque instability and rupture. The macrophage population is mainly ‘M1-like’. High numbers of dendritic cell with potential pro-inflammatory and anti-inflammatory functions are detected in the adventitia and atherosclerotic plaque. High numbers of interactions between antigen-specific T cells and antigen-presenting cells (dendritic cell and macrophages) are observed in plaque and adventitia. pDC, plasmacytoid dendritic cell, cDC, conventional dendritic cell, Mϕ, macrophage.
FIGURE 2
FIGURE 2
Proinflammatory and anti-inflammatory functions of macrophages and dendritic cells (DC) in atherosclerosis. (a) Atheroprotective mechanisms at early stages of atherosclerosis are mediated by anti-inflammatory functions of macrophages and DC, which includes induction of regulatory T cells (Treg) and anti-inflammatory cytokine production. The phagocytic function of macrophages contributes to clearance of dead cells and extracellular lipids. (b) During the later stages of atherosclerosis the proinflammatory mechanisms dominate. Both macrophages and dendritic cell produce proinflammatory cytokines and chemokines, which promote local inflammation. Antigen presentation is a signature of dendritic cells, however macrophages are able to present antigens to antigen-experienced T cells. Both macrophages and dendritic cells could become foam cells. Filled with lipids, foam cells can die forming the necrotic core inside the plaque, resulting in plaque instability and potential rupture.
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