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Erythrocyte-bound low-density lipoprotein immune complexes lead to cholesteryl ester accumulation in human

C Gisinger1, G T Virella, M F Lopes-Virella

  • 1Veterans Administration Medical Center, Charleston, South Carolina.

Clinical Immunology and Immunopathology
|April 1, 1991
PubMed

Insights

Immune complexes (IC) of low-density lipoproteins (LDL) bound to red blood cells (RBC) significantly increase cholesterol accumulation in macrophages. This process, mediated by Fc receptors, may contribute to atherosclerosis development.

Area of Science:

  • Immunology
  • Lipid Metabolism
  • Cardiovascular Research

Background:

  • Macrophages accumulate esterified cholesterol (CE) when incubated with insoluble immune complexes (IC) containing low-density lipoproteins (LDL).
  • This CE accumulation transforms macrophages into foam cells, a hallmark of atherosclerosis.

Purpose of the Study:

  • To investigate conditions promoting LDL-IC uptake and CE accumulation in macrophages.
  • To compare the effects of soluble, insoluble, and red blood cell (RBC)-bound LDL-IC on macrophage lipid metabolism.

Main Methods:

  • Studied uptake of labeled LDL-IC (using apoB or anti-LDL IgG) by human monocyte-derived macrophages (HMM).
  • Investigated the role of Fc receptors in LDL-IC ingestion using competition studies.
  • Quantified intracellular cholesteryl ester accumulation in HMM.

Main Results:

  • Uptake of LDL-IC by HMM was significantly enhanced when IC were adsorbed to RBC.
  • LDL-IC were ingested via the Fc receptor on HMM.
  • RBC-bound LDL-IC caused marked intracellular cholesteryl ester accumulation (78.4 ± 1.7 vs 5.5 ± 0.6 μg/mg cell protein), likely due to delayed LDL degradation.

Conclusions:

  • Macrophage uptake of LDL-IC is enhanced by RBC binding.
  • Ingestion of LDL as part of an antigen-antibody complex alters LDL metabolism.
  • Formation and RBC adsorption of LDL-IC may play a significant role in atherosclerosis onset and progression.

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