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Regulation of Class II Transactivator Promoter IV in Macrophages and Microglia: Involvement of the Suppressors of Cytokine Signaling-1 Protein
Department of Cell Biology, University of Alabama at Birmingham, Birmingham, AL 35294
The discovery of the class II transactivator (CIITA) transcription
factor, and its IFN-
-activated promoter (promoter IV), have provided
new opportunities to understand the molecular mechanisms of
IFN--induced class II MHC expression. Here, we investigated the
molecular regulation of IFN--induced murine CIITA promoter IV
activity in microglia/macrophages. In the macrophage cell line
RAW264.7, IFN- inducibility of CIITA promoter IV is dependent on an
IFN- activation sequence (GAS) element and adjacent E-Box, and an
IFN response factor (IRF) element, all within 196 bp of the
transcription start site. In both RAW cells and the microglia cell line
EOC20, two IFN--activated transcription factors, STAT-1
and
IRF-1, bind the GAS and IRF elements, respectively. The E-Box binds
upstream stimulating factor-1 (USF-1), a constitutively expressed
transcription factor. Functionally, the GAS, E-Box, and IRF elements
are each essential for IFN--induced CIITA promoter IV activity. The
effects of the suppressors of cytokine signaling-1 (SOCS-1) protein on
IFN--induced CIITA and class II MHC expression were examined.
Ectopic expression of SOCS-1 inhibits IFN--induced activation of
CIITA promoter IV and subsequent class II MHC protein expression.
Interestingly, SOCS-1 inhibits the constitutive expression of STAT-1
and its IFN--induced tyrosine phosphorylation and binding to the GAS
element in CIITA promoter IV. As well, IFN--induced expression of
IRF-1 and its binding to the IRF element is inhibited. These results
indicate that SOCS-1 may be responsible for attenuating IFN--induced
CIITA and class II MHC expression in
macrophages.
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