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Related Experiment Video

Updated: Apr 22, 2026

Quantification of Monocyte Transmigration and Foam Cell Formation from Individuals with Chronic Inflammatory Conditions
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Lymphocyte migration into atherosclerotic plaque.

Jie Li1, Klaus Ley2

  • 1From the Division of Inflammation Biology, La Jolla Institute for Allergy and Immunology, CA.

Arteriosclerosis, Thrombosis, and Vascular Biology
|October 11, 2014
PubMed
Summary

This review explores how T and B lymphocytes are recruited to atherosclerosis, focusing on specific chemokines and their receptors. Understanding lymphocyte homing is crucial for developing new atherosclerosis treatments.

Keywords:
CC chemokine receptoratherosclerosislymphocytes

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Area of Science:

  • Immunology
  • Cardiovascular Research
  • Pathogenesis of Atherosclerosis

Background:

  • Adaptive immunity plays a role in atherosclerosis development.
  • Lymphocyte recruitment to atherosclerotic lesions is less understood than monocyte recruitment.

Purpose of the Study:

  • To review the role of lymphocyte subsets in atherosclerosis pathogenesis.
  • To discuss chemokines and chemokine receptors involved in lymphocyte homing to atherosclerotic lesions.

Main Methods:

  • Literature review of current understanding.
  • Examination of evidence for specific chemokines (CCL5, CCL19, CCL21, CXCL10, CXCL16) and macrophage migration inhibitory factor.
  • Analysis of relevant chemokine receptors (CCR5, CCR6, CCR7, CXCR3, CXCR6, CXCR2/CXCR4) and L-selectin.

Main Results:

  • Several chemokines and their receptors are implicated in lymphocyte homing to atherosclerotic lesions.
  • L-selectin plays a role in mouse models of atherosclerosis.

Conclusions:

  • Lymphocyte recruitment is a key, yet understudied, aspect of atherosclerosis pathogenesis.
  • Targeting specific chemokine pathways may offer therapeutic strategies for atherosclerosis.