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Evidence for post‐transcriptional regulation of interleukin‐5 by dexamethasone
Author(s) -
Staples Karl J.,
Bergmann Martin W.,
Barnes Peter J.,
Newton Robert
Publication year - 2003
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1046/j.1365-2567.2003.01679.x
Subject(s) - peripheral blood mononuclear cell , phytohaemagglutinin , messenger rna , transfection , cytokine , transcription (linguistics) , dexamethasone , biology , transcriptional regulation , enhancer , microbiology and biotechnology , interleukin , interleukin 4 , gene expression , endocrinology , immunology , immune system , gene , in vitro , biochemistry , linguistics , philosophy
Summary Interleukin‐5 (IL‐5) is a T helper type 2 cytokine, which is implicated in the pathogenesis of eosinophilic diseases such as asthma. Both peripheral blood mononuclear cells (PBMC) and primary human T cells display similar patterns of IL‐5 expression when stimulated with both phorbol‐12‐myristate 13‐acetate and phytohaemagglutinin. The expression of IL‐5 stimulated by these agents was shown to require de novo transcription and translation. However, although dexamethasone was a potent inhibitor of both IL‐5 release and messenger RNA accumulation from PBMC and T cells, dexamethasone had no effect on the luciferase activity of a reporter construct under the control of an IL‐5 promoter region transiently transfected into primary human T cells. Furthermore, dexamethasone appeared to decrease the stability of IL‐5 messenger RNA and this effect was dependent upon de novo transcription. Taken together, the results presented here suggest that, whilst transcriptional processes predominantly regulate IL‐5 release, the mechanism by which dexamethasone inhibits IL‐5 is post‐transcriptional.