Fulltext

cAMP up-regulates IL-4 and IL-5 production from activated CD4+ T cells while decreasing IL-2 release and NF-AT induction

Lacour, Marc ; Arrighi, Jean-François ; Müller, Kai M. ; Cariberg, Carsten ; Saurat, Jean-Hilaire ; Hauser, Conrad

In: International Immunology, 1994, vol. 6, no. 9, p. 1333-1343

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    Titel
    • cAMP up-regulates IL-4 and IL-5 production from activated CD4+ T cells while decreasing IL-2 release and NF-AT induction
    Autor
    • Lacour, Marc. Department of Dermatology, Hôpital Cantonal Universitaire de Genėve, 24, rue Micheli-du-Crest, 1211 Geneva 14, Switzerland
    • Arrighi, Jean-François. Department of Dermatology, Hôpital Cantonal Universitaire de Genėve, 24, rue Micheli-du-Crest, 1211 Geneva 14, Switzerland
    • Müller, Kai M.. Department of Dermatology, Hôpital Cantonal Universitaire de Genėve, 24, rue Micheli-du-Crest, 1211 Geneva 14, Switzerland
    • Cariberg, Carsten. Department of Dermatology, Hôpital Cantonal Universitaire de Genėve, 24, rue Micheli-du-Crest, 1211 Geneva 14, Switzerland
    • Saurat, Jean-Hilaire. Department of Dermatology, Hôpital Cantonal Universitaire de Genėve, 24, rue Micheli-du-Crest, 1211 Geneva 14, Switzerland
    • Hauser, Conrad. Department of Dermatology, Hôpital Cantonal Universitaire de Genėve, 24, rue Micheli-du-Crest, 1211 Geneva 14, Switzerland
    Dokumententyp
    • Postprint
    Sprache
    • Englisch
    Veröffentlicht in
    • International Immunology, 1994, vol. 6, no. 9, p. 1333-1343. Oxford University Press
    Andere elektronische Ausgabe
    OAI-PMH-ID
    • oai:doc.rero.ch:291844
    Summary
    Seven days after activation with concanavalin A and irradiated spleen cells, murine CD4+ T cells were re-stimulated with lonomycin and phorbol 12-myristate 13-acetate (PMA). IL-2 and IL-4 were determined in the supernatant. When cholera toxin, forskolin together with phosphodlesterase inhibitors or dibutyryl-cAMP were added at the time of re-stimulation, a dose-dependent increase of IL-4 and IL-5 release was noted. IL-2 was down-regulated as reported before. The up-regulatlon of IL-4 and the down-regulation of IL-2 correlated with an increase of IL-4 mRNA and a decrease of IL-2 mRNA as determined by semi-quantitative reverse tratucriptase polymerase chain reaction. Similar results were found with prostaglandin E2 using PMA and ionomycin or plate-bound anti-CD3 antibody as re-stimulants. These results suggest that, in activated CD4+ T cells, cAMP-elevating agents induce a switch of lymphokine production towards a Th-like phenotype through regulation at the transcriptional level. This is supported by the fact that complex formation between a synthetic nuclear factor of activated T cells (NF-AT) binding site from the IL-2 promoter and nuclear extracts was decreased when cholera toxin was added to re-activated CD4+ T cells, suggesting that cholera toxin and cAMP down-regulate IL-2 expression via decreased NF-AT binding. Finally, since IL-4 has been reported to amplify IL-4 release from activated CD4+ T cells, the autoinduction of IL-4 may very well function via cAMP