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Journal of Lipid Research, Vol. 42, 1913-1922, November 2001
Copyright © 2001 by Lipid Research, Inc.

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

Correspondence to: Allison B. Reiss, To whom correspondence should be addressed., reissa01{at}popmail.med.nyu.edu (E-mail)

The enzyme cholesterol 27-hydroxylase, expressed by arterial endothelium and monocytes/macrophages, is one of the first lines of defense against the development of atherosclerosis. By catalyzing the hydroxylation of cholesterol to 27-hydroxycholesterol, which is more soluble in aqueous medium, the enzyme promotes the removal of cholesterol from the arterial wall. Prior studies have suggested that immune reactants play a role in the pathogenesis of atherosclerosis; we report here that immune reactants, IFN- and immune complexes bound to C1q, but not interleukin-1 and tumor necrosis factor, diminish the expression of cholesterol 27-hydroxylase in human aortic endothelial cells, peripheral blood mononuclear cells, monocyte-derived macrophages, and the human monocytoid cell line THP-1. In addition, our studies demonstrate that immune complexes down-regulate cholesterol 27-hydroxylase only after complement fixation via interaction with the 126-kD C1qRp protein on endothelial cells and THP-1 cells.

These results are consistent with the prior demonstration that IFN- contributes to the pathogenesis of atherosclerosis and suggest a role for C1q receptors in the atherogenic process. Moreover, these observations suggest that one mechanism by which immune reactants contribute to the development of atherosclerosis is by down-regulating the expression of the enzymes required to maintain cholesterol homeostasis in the arterial wall. — Reiss, A. B., N. W. Awadallah, S. Malhotra, M. C. Montesinos, E. S. L. Chan, N. B. Javitt, and B. N. Cronstein. Immune complexes and IFN- decrease cholesterol 27-hydroxylase in human arterial endothelium and macrophages. J. Lipid Res. 2001. 42: 1913–1922.

Supplementary key words: atherosclerosis, complement 1q, cytokines, 27-hydroxycholesterol

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