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Regulation of the Type IV Class II Transactivator Promoter in Astrocytes1
Departments of
*
Cell Biology and
Physiology and Biophysics, University of Alabama, Birmingham, AL 35294
The transcriptional activation of class II MHC genes requires the
class II transactivator (CIITA) protein, a regulator that is essential
for both constitutive and IFN-
-inducible class II MHC expression.
The CIITA gene is controlled by multiple independent promoters; two
promoters direct constitutive expression, while another, the type IV
CIITA promoter, mediates IFN--induced expression. We investigated
the molecular regulation of IFN--induced type IV CIITA promoter
activity in astrocytes. IFN- inducibility of the type IV CIITA
promoter is dependent on three cis-acting elements
contained within a 154-bp fragment of the promoter; the proximal
IFN- activation sequence (GAS) element, the E box, and the proximal
IFN regulatory factor (IRF) element. Two IFN--activated
transcription factors, STAT-1
and IRF-1, bind the proximal GAS and
IRF elements, respectively. The E box binds upstream stimulating
factor-1 (USF-1), a constitutively expressed transcription factor.
Furthermore, STAT-1 binding to the proximal GAS element is dependent
on the binding of USF-1 to the adjacent E box. Functionally, the
proximal IRF element is essential for IFN- induction of type IV
CIITA promoter activity, while the proximal GAS and E box elements
contribute to the IFN- inducibility of this promoter. In astrocytes,
TNF- enhances IFN--induced class II MHC transcription. Our
results demonstrate that TNF- does not enhance IFN--induced
transcriptional activation of the type IV CIITA promoter, indicating
that the enhancing effect of TNF- is mediated downstream of CIITA
transcription. These results define the molecular basis of IFN-
activation of the type IV CIITA promoter in
astrocytes.
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