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J. Biol. Chem., Vol. 266, Issue 33, 22079-22082, 11, 1991
MA Cassatella, F Bazzoni, F Calzetti, I Guasparri, F Rossi and G Trinchieri
We examined the mechanisms responsible for the regulation by interferon-
gamma (IFN-gamma) of the expression of the genes encoding the high affinity
IgG-Fc receptor (Fc gamma R-I, CD64) and the NADPH oxidase 47- kDa
cytosolic factor (p47-phox) in human polymorphonuclear leukocytes (PMN).
Nuclear run-on transcriptional assays demonstrated that the Fc gamma R-I
gene transcription is undetectable in untreated PMN but is significantly
induced by IFN-gamma. Unlike Fc gamma R-I, p47-phox gene transcription is
constitutively active in resting PMN and is down- regulated by a 2-h
treatment of these cells with IFN-gamma. The transcriptional modulation by
IFN-gamma of Fc gamma R-I and p47-phox genes is not influenced by the
protein synthesis inhibitor cycloheximide. Moreover, Northern blot analysis
revealed that cycloheximide superinduces p47-phox mRNA expression by
increasing its half-life and without affecting p47-phox gene transcription.
These findings indicate that human PMN can regulate gene expression by
transcriptional and posttranscriptional events.
Interferon-gamma transcriptionally modulates the expression of the genes for the high affinity IgG-Fc receptor and the 47-kDa cytosolic component of NADPH oxidase in human polymorphonuclear leukocytes
Institute of General Pathology, Universita di Verona, Italy.
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