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Interleukin-10 inhibits interferon-gamma-induced intercellular adhesion
molecule-1 gene transcription in human monocytes
S Song, H Ling-Hu, KA Roebuck, MF Rabbi, RP Donnelly and A Finnegan
Department of Medicine, Rush Presbyterian-St Luke's Medical Center,
Chicago, IL 60612, USA.
Interleukin-10 (IL-10) is a potent monocyte regulatory cytokine that
inhibits gene expression of proinflammatory mediators. In this study, we
investigated the mechanism by which IL-10 downregulates expression of
intercellular adhesion molecule-1 (ICAM-1) on the cell surface of normal
human monocytes activated with interferon-gamma (IFN-gamma). IL- 10
inhibition of IFN-gamma-induced ICAM-1 expression was apparent as early as
3 hours and was blocked by an anti-IL-10 antibody but not by an
isotype-matched control antibody. Northern blot analysis showed that IL-10
reduced the accumulation of ICAM-1 mRNA in IFN-gamma-stimulated monocytes.
IL-10 inhibition of ICAM-1 steady-state mRNA was detected at 3 hours and
remained at 24 hours. Nuclear run-on transcription assays showed that IL-10
inhibited the rate of IFN-gamma-induced transcription of the ICAM-1 gene,
and mRNA stability studies showed that IL-10 did not alter the half-life of
IFN-gamma-induced ICAM-1 message. Thus, IL- 10 inhibits IFN-gamma-induced
ICAM-1 expression in monocytes primarily at the level of gene
transcription. Activation of IFN-gamma-responsive genes requires tyrosine
phosphorylation of the transcriptional factor STAT-1alpha (signal
transducer and activator of transcription-1alpha). However, IL-10 did not
affect IFN-gamma-induced tyrosine phosphorylation of STAT-1alpha or alter
STAT-1alpha binding to the IFN- gamma response element (IRE) in the ICAM-1
promoter. Instead, IL-10 prevented IFN-gamma-induced binding activity at
the NF-kappaB site of the tumor necrosis factor alpha
(TNF-alpha)-responsive NF-kappaB/C-EBP composite element in the ICAM-1
promoter. These data indicate that IL- 10 inhibits IFN-gamma-induced
transcription of the ICAM-1 gene by a regulatory mechanism that may involve
NF-kappaB.
Volume 89,
Issue 12,
pp. 4461-4469,
06/15/1997
Copyright © 1997 by The American Society of Hematology
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