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Receptor I in Monocytes1
*
Institute of Medical Technology, and Department of Medical Biochemistry, University of Tampere, and
Department of Clinical Microbiology, Tampere University Hospital, Tampere, Finland;
Chemotherapeutisches Forschungsinstitut, Georg Speyer Haus, Frankfurt am Main, Germany; and
§
Institute of Biomedicine, Departments of Physiology and Clinical Chemistry, University of Helsinki, Helsinki, Finland
IFN-
and glucocorticoids regulate inflammatory and immune
responses through Stat1 and glucocorticoid receptor (GR) transcription
factors, respectively. The biological responses to these polypeptides
are determined by integration of various signaling pathways in a
cell-type and promoter-dependent manner. In this study we have
characterized the molecular basis for the functional cooperation
between IFN- and dexamethasone (Dex) in the induction of the
high-affinity Fc receptor I (FcRI) in monocytes. Dex did not
affect IFN--induced Stat1 DNA binding activity or induce novel
DNA-binding complexes to the FcRI promoter. By using cell systems
lacking functional GR or Stat1, we showed that GR stimulated
Stat1-dependent transcription in a ligand-dependent manner, while Stat1
did not influence GR-dependent transcription. The cooperation required
phosphorylation of Tyr701, DNA binding, and the
trans-activation domain of Stat1, but did not involve
Ser727 phosphorylation of Stat1 or physical interaction
between GR and Stat1. The costimulatory effect of Dex was not dependent
on a consensus glucocorticoid response element in the Stat1-responsive
promoters, but required the DNA-binding and
trans-activation functions of GR, and Dex-induced
protein synthesis. GR activated the natural FcRI promoter construct,
and this response required both Stat1 and the Ets family transcription
factor PU.1. Previously, physical association between GR and Stat5 has
been shown to enhance Stat5-dependent and suppress GR-dependent
transcription. The results shown here demonstrate a distinct, indirect
mechanism of cross-modulation between cytokine and steroid receptor
signaling that integrates Stat1 and GR pathways with cell type-specific
PU.1 transcription factor in the regulation of FcRI gene
transcription.
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