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Interferon-
These results suggest a model involving the
inhibition of IFN-
Volume 270,
Number 21,
Issue of May 26, pp. 12548-12556, 1995
©1995 by The American Society for Biochemistry and Molecular Biology, Inc.
Promoter by
Glucocorticoids and Dominant Negative Mutants of c-Jun
(IFN-
) is an immunoregulatory cytokine
expressed in large granular lymphocytes and T cells. However, the
molecular mechanisms underlying IFN-
gene transcription have not
been fully defined. Here, we analyze the mechanisms responsible for the
inhibition of IFN-
promoter activity by the glucocorticoid hormone
dexamethasone. Cotransfection assays performed in Jurkat T cells
demonstrated that the activity of the initial 108 base pairs of the
IFN-
promoter was down-regulated in the presence of dexamethasone.
Furthermore, utilizing electrophoretic mobility shift analysis, we
identified activator protein 1 AP-1-cAMP response element binding
protein-activating transcription factor (CREB-ATF) binding elements
situated in positions of the IFN-
promoter previously identified
as essential for promoter activity. Moreover, dominant negative mutants
of the c-Jun proto-oncogene were able to mimic the same down-regulatory
effect exerted by dexamethasone, and mutations that abolished the
binding of the AP-1
CREB-ATF factors were able to block the
glucocorticoid effect.
AP-1
CREB-ATF DNA binding complexes as one
of the mechanisms involved in the negative regulatory action of
glucocorticoids on IFN-
gene expression and support the relevance
of AP-1
CREB-ATF binding factors during the transcriptional
activation of the IFN-
promoter in T cells.
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