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Regulation of cytokine and cytokine receptor expression by glucocorticoids
Author(s) -
Almawi Wassim Y.,
Beyhum Hayfa N.,
Rahme Amal A.,
Rieder Michael J.
Publication year - 1996
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.60.5.563
Subject(s) - biology , cytokine , cytokine receptor , transcription factor , glucocorticoid , glucocorticoid receptor , microbiology and biotechnology , receptor , immunology , gene , genetics
Glucocorticoids (GCS) profoundly inhibit several aspects of T cell immunity largely through inhibition of cytokine expression at the transcriptional and posttranscriptional levels. GCS were also reported to act indirectly by inducing transforming growth factor‐β expression, which in turn blocks T cell immunity. In exerting their antiproliferative effects, GCS diffuse into target cells where they bind their cytoplasmic receptor, which in turn translocates to the nucleus where it inhibits transcription of cytokine genes through direct binding to the glucocorticoid response elements (GRE), which are located in the promoter region of cytokine genes or, alternatively, through antagonism of the action of transcription factors required for optimal transcriptional activation. In contrast to their inhibitory effects on cytokine expression, GCS upregulate cytokine receptor expression that correlates with enhanced cytokine effects on target cells. In this review, we summarize the current state of knowledge of the mechanism of action of GCS, including the phenomenon of steroid‐induced rebound, which ensues upon GCS withdrawal. J. Leukoc. Biol . 60: 563–572; 1996.