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Department of Molecular Biology University of Gent-VIB 9000 Gent, Belgium
Interleukin-6 (IL-6) is a pleiotropic cytokine
that is involved in many autoimmune and inflammatory diseases.
Transcriptional control of IL-6 gene expression is exerted by various
compounds, among which glucocorticoids are the most potent
antiinflammatory and immunosuppressive agents currently in use.
Glucocorticoids exert their transrepressive actions by negatively
interfering with transcription factors, such as nuclear factor-
B
(NF-B) and AP-1. Both factors make use of the coactivator cAMP
response element-binding protein (CREB)-binding protein (CBP) to
enhance their transcriptional activities, which led to the hypothesis
that a mutual antagonism between p65 or c-Jun and activated
glucocorticoid receptor (GR) results from a limited amount of
CBP. Recently, we showed that glucocorticoid repression of
NF-B-driven gene expression occurs irrespective of the amount of
coactivator levels in the cell. In the current study, we extend this
observation and demonstrate that also AP-1-targeted gene repression by
glucocorticoids is refractory to increased amounts of nuclear
coactivators. From results with Gal4 chimeric proteins we conclude that
glucocorticoid repression occurs by a promoter-independent mechanism
involving a nuclear interplay between activated GR and AP-1,
independently of CBP levels in the cell.
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