Evidence for post-transcriptional regulation of interleukin-5 by dexamethasone

Staples, Karl J., Bergmann, Martin W., Barnes, Peter J. and Newton, Robert (2003) Evidence for post-transcriptional regulation of interleukin-5 by dexamethasone. Immunology, 109 (4), 527-535. (doi:10.1046/j.1365-2567.2003.01679.x). (PMID:12871219)

Abstract

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

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Contributors

Author: Karl J. Staples

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