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Immune complexes and IFN-gamma decrease cholesterol 27-hydroxylase in human arterial endothelium and macrophages.

A B Reiss1, N W Awadallah, S Malhotra

  • 1Department of Medicine, New Bellevue 16N28, New York University School of Medicine, 550 First Avenue, New York, NY 10016, USA. reissa01@popmail.med.nyu.edu

Journal of Lipid Research
|November 21, 2001
PubMed
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Immune reactants like IFN-gamma and C1q-bound immune complexes reduce cholesterol 27-hydroxylase expression, hindering cholesterol removal and potentially contributing to atherosclerosis development.

Area of Science:

  • Biochemistry
  • Immunology
  • Cardiovascular Research

Background:

  • Cholesterol 27-hydroxylase is crucial for removing arterial cholesterol, acting as a defense against atherosclerosis.
  • Immune system involvement in atherosclerosis pathogenesis is increasingly recognized.

Purpose of the Study:

  • To investigate the impact of specific immune reactants on cholesterol 27-hydroxylase expression in cells relevant to atherosclerosis.
  • To elucidate the role of complement fixation and C1q receptors in this immune-mediated regulation.

Main Methods:

  • Assessing the effect of interferon-gamma (IFN-gamma) and immune complexes (ICs) on cholesterol 27-hydroxylase expression.
  • Utilizing human aortic endothelial cells, peripheral blood mononuclear cells, macrophages, and THP-1 cell line.

Related Experiment Videos

  • Investigating the role of complement fixation and C1q receptor (C1qRp) interaction.

    • Main Results:

    • IFN-gamma and C1q-bound ICs, but not IL-1 or TNF, significantly diminished cholesterol 27-hydroxylase expression.
    • Immune complex-mediated down-regulation required complement fixation and interaction with C1qRp.
    • These effects were observed across multiple cell types, including endothelial cells and macrophages.

    Conclusions:

    • Specific immune reactants can impair the body's cholesterol-clearing mechanisms in the arterial wall.
    • C1q receptors and complement fixation are implicated in the atherogenic effects of immune complexes.
    • Down-regulation of cholesterol 27-hydroxylase by immune factors represents a potential mechanism driving atherosclerosis development.