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Citations to this article

Interferon-gamma inhibits scavenger receptor expression and foam cell formation in human monocyte-derived macrophages.
Y J Geng, G K Hansson
Y J Geng, G K Hansson
Published April 1, 1992
Citation Information: J Clin Invest. 1992;89(4):1322-1330. https://doi.org/10.1172/JCI115718.
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Research Article Article has an altmetric score of 3

Interferon-gamma inhibits scavenger receptor expression and foam cell formation in human monocyte-derived macrophages.

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Abstract

The scavenger receptor (ScR) mediates uptake of chemically modified low density lipoprotein (LDL) by human monocyte-derived macrophages. It is not down-regulated by high intracellular cholesterol levels, and exposure of macrophages to acetylated or oxidized LDL therefore leads to foam cell development. The hypothesis that this represents an important mechanism for intracellular cholesterol accumulation in atherosclerosis is supported by the finding of ScR expression in foam cells of atherosclerotic plaques. T lymphocytes are also present in such plaques and it is known that T cell products regulate macrophage activation. We have therefore studied the effect of interferon-gamma (IFN gamma), a lymphokine secreted by activated T lymphocytes, on the expression of ScR in human monocyte-derived macrophages. Binding and uptake of acetylated LDL were significantly reduced in macrophages exposed to recombinant IFN gamma or IFN gamma-containing lymphocyte-conditioned media. Competition experiments showed that the IFN gamma-regulated binding and uptake of acetylated LDL was mediated via ScR. IFN gamma exerted its effect on the saturable binding of acetylated LDL by reducing the number of cell surface binding sites without significantly affecting the affinity between acetylated LDL and its receptor. Northern analysis revealed that the type I ScR mRNA was significantly reduced in IFN gamma-treated cells. Finally, IFN gamma treatment reduced intracellular cholesteryl ester accumulation and inhibited the development of foam cells in the cultures. In conclusion, our data show that IFN gamma blocks the development of macrophage-derived foam cells by inhibiting expression of ScR. This suggests that macrophage-T lymphocyte interactions may reduce intracellular cholesterol accumulation in the atherosclerotic plaque.

Authors

Y J Geng, G K Hansson

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Year: 2024 2022 2021 2020 2019 2018 2015 2014 2013 2012 2011 2010 2009 2008 2006 2005 2004 2003 2002 2001 2000 1999 1998 1997 1996 1995 1994 1993 1992 1991 1949 Total
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Citations to this article in year 2002 (8)

Title and authors Publication Year
Macrophages, Oxidation, and Endometriosis
N Santanam, AA Murphy, S Parthasarathy
Annals of the New York Academy of Sciences 2002
Cruzipain, a majorTrypanosoma cruziantigen, conditions the host immune response in favor of parasite
L Giordanengo, N Guiñazú, C Stempin, R Fretes, F Cerbán, S Gea
European Journal of Immunology 2002
Human macrophage-induced vascular smooth muscle cell apoptosis requires NO enhancement of Fas/Fas-L interactions
JJ Boyle, PL Weissberg, MR Bennett
Arteriosclerosis, thrombosis, and vascular biology 2002
A Novel Role of Sp1 and Sp3 in the Interferon-γ-mediated Suppression of Macrophage Lipoprotein Lipase Gene Transcription
TR Hughes, TS Tengku-Muhammad, SA Irvine, DP Ramji
The Journal of biological chemistry 2002
Class A scavenger receptors mediate cell adhesion via activation of G i/o and formation of focal adhesion complexes
SR Post, C Gass, S Rice, D Nikolic, H Crump, GR Post
Journal of lipid research 2002
Interferon-γ–Mediated Downregulation of Cholesterol Efflux and ABC1 Expression Is by the Stat1 Pathway
XQ Wang, CG Panousis, ML Alfaro, GF Evans, SH Zuckerman
Arteriosclerosis, thrombosis, and vascular biology 2002
Activation of the Stem Cell-Derived Tyrosine Kinase/RON Receptor Tyrosine Kinase by Macrophage-Stimulating Protein Results in the Induction of Arginase Activity in Murine Peritoneal Macrophages
AC Morrison, PH Correll
Journal of immunology (Baltimore, Md. : 1950) 2002
Blockade of B7/CD28 in mixed lymphocyte reaction cultures results in the generation of alternatively activated macrophages, which suppress T-cell responses
D Tzachanis, A Berezovskaya, LM Nadler, VA Boussiotis
Blood 2002

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