Evidence for post-transcriptional regulation of interleukin-5 by dexamethasone
UNSPECIFIED. (2003) Evidence for post-transcriptional regulation of interleukin-5 by dexamethasone. IMMUNOLOGY, 109 (4). pp. 527-535. ISSN 0019-2805Full text not available from this repository.
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.
|Item Type:||Journal Article|
|Subjects:||Q Science > QR Microbiology > QR180 Immunology|
|Journal or Publication Title:||IMMUNOLOGY|
|Publisher:||BLACKWELL PUBLISHING LTD|
|Number of Pages:||9|
|Page Range:||pp. 527-535|
Actions (login required)