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Interferon-gamma increases the expression of the gene encoding the beta
subunit of the granulocyte-macrophage colony-stimulating factor receptor
M Hallek, EM Lepisto, KE Slattery, JD Griffin and TJ Ernst
Division of Tumor Immunology, Dana-Farber Cancer Institute, Boston, MA
02115.
Granulocyte-macrophage colony-stimulating factor (GM-CSF) activates a broad
range of myeloid cells through binding to high-affinity receptors
(GM-CSF-R) consisting of at least two distinct subunits, GM-CSF-R alpha and
GM-CSF-R beta. The genes of these GM-CSF-R subunits have been identified
recently, but little is known about the regulation of their expression. In
this study, we investigated the expression of the GM-CSF- R subunit genes
in normal human monocytes. Out of a panel of various cytokines and factors
tested, only interferon-gamma (IFN-gamma) affected the expression of one of
the GM-CSF-R subunit genes by increasing the GM-CSF-R beta mRNA expression
threefold to sixfold with no effect on GM-CSF-R alpha. Maximal effects
occurred 2 to 4 hours after stimulation with 500 to 5,000 U/mL IFN-gamma.
Nuclear run-on assays and mRNA half-life studies showed that IFN-gamma
modestly enhanced the transcription of the GM-CSF-R beta gene and
stabilized the GM-CSF-R beta mRNA, with the latter mechanism predominant.
Pretreatment of the monocytes with cycloheximide did not abrogate the
increase of GM- CSF-R beta mRNA expression induced by IFN-gamma, indicating
that de novo protein synthesis was not required for this activity. When
monocytes were exposed to IFN-gamma for 6 to 24 hours, the number of GM-
CSF-R per cell was increased 79% as compared with controls, whereas the
receptor affinity remained unchanged. These data indicate that the GM-
CSF-R expression in monocytes may be upregulated by IFN-gamma via an
increased expression of the beta subunit gene, involving both
transcriptional and post-transcriptional mechanisms.
Volume 80,
Issue 7,
pp. 1736-1742,
10/01/1992
Copyright © 1992 by The American Society of Hematology
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