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Stimulus-specific inhibition of IL-5 by cAMP-elevating agents and IL-10 reveals differential mechanisms of action

Stimulus-specific inhibition of IL-5 by cAMP-elevating agents and IL-10 reveals differential mechanisms of action
Stimulus-specific inhibition of IL-5 by cAMP-elevating agents and IL-10 reveals differential mechanisms of action
Interleukin-5 (IL-5) is a Th2 cytokine, which is implicated in the pathogenesis of eosinophilic diseases such as asthma. Peripheral blood mononuclear cells (PBMC), costimulated with phorbol 12-myristate 13-acetate (PMA) plus phytohemagglutinin (PHA) or activating antibodies to the CD3 and CD28 T-lymphocyte surface markers, produced similar patterns of IL-5 expression. However, in PMA + PHA-treated cells, 8-bromo-cAMP and PGE2 did not affect IL-5 expression, whereas in CD3 + CD28-stimulated cells, almost total repression was observed. IL-10 failed to inhibit IL-5 mRNA from PMA + PHA-treated cells, yet reduced release by 40%. By contrast, IL-10 totally inhibited CD3 + CD28-induced IL-5 release and inhibited mRNA by 50–60%. These results highlight important biological differences in the induction of IL-5 by the nonspecific stimulus PMA + PHA and the more physiological CD3 + CD28 costimulation. Finally, the potential for downregulating Th2 responses by cAMP-elevating agents or IL-10 is demonstrated and a significant role for posttranscriptional mechanisms in the inhibition by IL-10 is suggested
0006-291X
811-815
Staples, Karl J.
e0e9d80f-0aed-435f-bd75-0c8818491fee
Bergmann, Martin
6d5bd707-d510-415c-bade-02b2caafa050
Barnes, Peter J.
6cbf850c-3499-4e23-983c-4442643c0004
Newton, Robert
4a2c2a99-b7ad-4373-8840-96fbb5b5313e
Staples, Karl J.
e0e9d80f-0aed-435f-bd75-0c8818491fee
Bergmann, Martin
6d5bd707-d510-415c-bade-02b2caafa050
Barnes, Peter J.
6cbf850c-3499-4e23-983c-4442643c0004
Newton, Robert
4a2c2a99-b7ad-4373-8840-96fbb5b5313e

Staples, Karl J., Bergmann, Martin, Barnes, Peter J. and Newton, Robert (2000) Stimulus-specific inhibition of IL-5 by cAMP-elevating agents and IL-10 reveals differential mechanisms of action. Biochemical and Biophysical Research Communications, 273 (3), 811-815. (doi:10.1006/bbrc.2000.3023). (PMID:10891328)

Record type: Article

Abstract

Interleukin-5 (IL-5) is a Th2 cytokine, which is implicated in the pathogenesis of eosinophilic diseases such as asthma. Peripheral blood mononuclear cells (PBMC), costimulated with phorbol 12-myristate 13-acetate (PMA) plus phytohemagglutinin (PHA) or activating antibodies to the CD3 and CD28 T-lymphocyte surface markers, produced similar patterns of IL-5 expression. However, in PMA + PHA-treated cells, 8-bromo-cAMP and PGE2 did not affect IL-5 expression, whereas in CD3 + CD28-stimulated cells, almost total repression was observed. IL-10 failed to inhibit IL-5 mRNA from PMA + PHA-treated cells, yet reduced release by 40%. By contrast, IL-10 totally inhibited CD3 + CD28-induced IL-5 release and inhibited mRNA by 50–60%. These results highlight important biological differences in the induction of IL-5 by the nonspecific stimulus PMA + PHA and the more physiological CD3 + CD28 costimulation. Finally, the potential for downregulating Th2 responses by cAMP-elevating agents or IL-10 is demonstrated and a significant role for posttranscriptional mechanisms in the inhibition by IL-10 is suggested

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Published date: 14 July 2000
Organisations: Faculty of Medicine

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Local EPrints ID: 374424
URI: http://eprints.soton.ac.uk/id/eprint/374424
ISSN: 0006-291X
PURE UUID: 08be8cac-98f3-4944-aa94-21bfe47db3b3
ORCID for Karl J. Staples: ORCID iD orcid.org/0000-0003-3844-6457

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Date deposited: 16 Feb 2015 14:44
Last modified: 26 Nov 2019 01:44

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Author: Karl J. Staples ORCID iD
Author: Martin Bergmann
Author: Peter J. Barnes
Author: Robert Newton

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