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Updated: May 31, 2026
Quantification of Monocyte Transmigration and Foam Cell Formation from Individuals with Chronic Inflammatory Conditions
Published on: October 17, 2017
Monocyte and macrophage dynamics during atherogenesis
Klaus Ley1, Yury I Miller, Catherine C Hedrick
1Division of Inflammation Biology, La Jolla Institute for Allergy and Immunology, La Jolla, CA 92037, USA. klaus@liai.org
Insights
Monocyte influx into blood vessels drives atherosclerosis, a common vascular inflammation. These monocytes become inflammatory macrophages, contributing to lesion development and progression.
Area of Science:
- Immunology
- Cardiovascular Biology
- Cell Biology
Background:
- Vascular inflammation, particularly atherosclerosis, involves leukocyte dynamics within the vessel wall.
- Resident macrophages and dendritic cells exist in the arterial wall, but monocyte recruitment is critical during atherosclerosis.
Purpose of the Study:
- To review the role of monocyte influx and differentiation in the initiation and progression of atherosclerosis.
- To discuss the phenotypic modulation and fate of monocytic cells within the vascular wall.
Main Methods:
- Review of existing literature on monocyte subsets (Ly-6C(+) and Ly-6C(-)) in atherosclerosis.
- Analysis of factors influencing monocyte differentiation and macrophage phenotype.
- Examination of monocyte-derived macrophage apoptosis, efferocytosis, and secondary necrosis.
Main Results:
- Atherosclerosis induces rapid influx of inflammatory monocytes (Ly-6C(+) in mice) and patrolling monocytes (Ly-6C(-) in mice).
- Recruited monocytes differentiate into inflammatory macrophages and dendritic cells, influenced by various molecular signals.
- Monocyte-derived macrophages undergo apoptosis, with efferocytosis or secondary necrosis impacting atherosclerotic lesion development.
Conclusions:
- Monocytic cell dynamics are central to the pathogenesis of atherosclerosis.
- Understanding these processes is crucial for developing targeted therapies for vascular inflammation.
Abstract:
Vascular inflammation is associated with and in large part driven by changes in the leukocyte compartment of the vessel wall. Here, we focus on monocyte influx during atherosclerosis, the most common form of vascular inflammation. Although the arterial wall contains a large number of resident macrophages and some resident dendritic cells, atherosclerosis drives a rapid influx of inflammatory monocytes (Ly-6C(+) in mice) and other monocytes (Ly-6C(-) in mice, also known as patrolling monocytes). Once in the vessel wall, Ly-6C(+) monocytes differentiate to a phenotype consistent with inflammatory macrophages and inflammatory dendritic cells. The phenotype of these cells is modulated by lipid uptake, Toll-like receptor ligands, hematopoietic growth factors, cytokines, and chemokines. In addition to newly recruited macrophages, it is likely that resident macrophages also change their phenotype. Monocyte-derived inflammatory macrophages have a short half-life. After undergoing apoptosis, they may be taken up by surrounding macrophages or, if the phagocytic capacity is overwhelmed, can undergo secondary necrosis, a key event in forming the necrotic core of atherosclerotic lesions. In this review, we discuss these and other processes associated with monocytic cell dynamics in the vascular wall and their role in the initiation and progression of atherosclerosis.
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