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Down regulation of CD11b and CD18 expression in atherosclerotic lesion-derived macrophages

J L Gray1, R Shankar

  • 1Department of Surgery, Loyola University Medical Center, Maywood, Illinois, USA.

The American Surgeon
|August 1, 1995
PubMed

Insights

Reduced CD11b/CD18 integrin expression on macrophages may prevent their exit from atherosclerotic lesions. This study investigated CD11b and CD18 levels in normal monocytes versus lesion-derived macrophages in rabbits, finding significantly lower expression in lesion macrophages.

Area of Science:

  • Immunology
  • Cardiovascular Research
  • Cell Biology

Background:

  • Monocyte/macrophages are crucial in atherosclerosis development.
  • Reverse monocyte traffic from lesions to circulation ceases as lesions progress.
  • Reduced CD11b/CD18 integrin expression is hypothesized to impede monocyte/macrophage exit from lesions.

Purpose of the Study:

  • To compare CD11b and CD18 expression in normal rabbit monocytes (NMø) and atherosclerotic lesion-derived macrophages (AthMø).
  • To investigate the role of CD11b/CD18 integrins in monocyte/macrophage egress from atherosclerotic plaques.

Main Methods:

  • Isolated AthMø from aortic lesions of rabbits on a high-cholesterol diet post-angioplasty.
  • Utilized anti-CD11b and anti-CD18 antibody staining.
  • Employed flow cytometry and immunohistochemical staining for analysis.
  • Separated AthMø based on size and granularity.

Main Results:

  • Normal monocytes (NMø) exhibited strong surface expression of CD11b and CD18.
  • Smaller, less granular AthMø showed minimal CD11b/CD18 expression (<1%).
  • Larger, more granular AthMø had reduced CD18 expression (37%) compared to NMø (>90%).

Conclusions:

  • Atherosclerotic lesion-derived macrophages display significantly reduced CD11b/CD18 integrin expression compared to normal monocytes.
  • This downregulation of CD11b/CD18 may impair the ability of macrophages to exit atherosclerotic lesions.
  • Findings suggest a mechanism contributing to the retention of macrophages within developing atherosclerotic plaques.

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