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Inhibition of Class II Transactivator and Class II MHC Expression1
*
Department of Cell Biology, University of Alabama, Birmingham, AL 35294; and
Laboratory of Cell Regulation and Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892
TGF-
is a immunoregulatory cytokine that inhibits class II MHC
expression in a variety of cell types. Previous studies have shown that
the class II MHC transactivator (CIITA), a master regulator that
controls class II MHC expression, is targeted by TGF- for repression
of IFN-
-induced class II MHC expression in astrocytes. The
mechanism(s) underlying the TGF- inhibitory effect is not
understood. In this study, we demonstrate that TGF- inhibition of
CIITA expression occurs at the transcriptional level, and that both
constitutive and IFN--induced human CIITA type IV promoter activity
is inhibited by TGF-. TGF- does not affect the signaling events
that mediate IFN- activation of CIITA expression; i.e, TGF- does
not inhibit IFN--induced STAT-1
phosphorylation and/or DNA
binding ability, nor is IFN- induction of IFN regulatory factor
affected. The inhibitory effect of TGF- on the type IV CIITA
promoter is mediated through a promoter region within 80 bp from the
transcription start site. Elimination of TGF- inhibition of class II
MHC and CIITA expression in Smad3-deficient astrocytes, as well as
restoration of the inhibitory effect by overexpression of the Smad3
protein, demonstrates that Smad3 is essential in mediating TGF-
inhibition of CIITA and class II MHC expression.
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