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Related Experiment Video

Updated: May 31, 2026

Quantification of Monocyte Transmigration and Foam Cell Formation from Individuals with Chronic Inflammatory Conditions
09:41

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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

Arteriosclerosis, Thrombosis, and Vascular Biology
|June 17, 2011
PubMed
Summary

Monocyte influx into blood vessels drives atherosclerosis, a common vascular inflammation. These monocytes become inflammatory macrophages, contributing to lesion development and progression.

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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.