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J. Biol. Chem., Vol. 277, Issue 49, 47022-47027, December 6, 2002

This Article Full Text Full Text (PDF) All Versions of this Article: 277/49/47022    most recent M207414200v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Schwenger, G. T. F. Articles by Mordvinov, V. A. Search for Related Content PubMed PubMed Citation Articles by Schwenger, G. T. F. Articles by Mordvinov, V. A. Social Bookmarking                      What's this?

Specific Activation of Human Interleukin-5 Depends on de Novo Synthesis of an AP-1 Complex^*

Gretchen T. F. Schwenger^§, Chee Choy Kok, Estri Arthaningtyas, Marc A. Thomas^¶, Colin J. Sanderson, and Viatcheslav A. Mordvinov^**

From the  Western Australian Institute for Medical Research and the School of Biomedical Sciences, Curtin University of Technology, Perth, Western Australia 6000, Australia ^¶ Institut de Pharmacologie and Toxicologie, Université de Lausanne, CH-1005 Switzerland, and ^** Universite Libre de Bruxelles, Faculte de Medecine, Laboratoire d'Immunologie experimentale, CP615, 808 Route de Lennik, B1070 Brussels, Belgium

It is clear from the biology of eosinophilia that a specific regulatory mechanism must exist. Because interleukin-5 (IL5) is the key regulatory cytokine, it follows that a gene-specific control of IL5 expression must exist that differs even from closely related cytokines such as IL4. Two features of IL5 induction make it unique compared with other cytokines; first, induction by cyclic adenosine monophosphate (cAMP), which inhibits other T-cell-derived cytokines, and second, sensitivity to protein synthesis inhibitors, which have no effect on other cytokines. This study has utilized the activation of different transcription factors by different stimuli in a human T-cell line to study the role of conserved lymphokine element 0 (CLE0) in the specific induction of IL5. In unstimulated cells the ubiquitous Oct-1 binds to CLE0. Stimulation induces de novo synthesis of the AP-1 members JunD and Fra-2, which bind to CLE0. The amount of IL5 produced correlates with the production of the AP-1 complex, suggesting a key role in IL5 expression. The formation of the AP-1 complex is essential, but the rate-limiting step is the synthesis of AP-1, especially Fra-2. This provides an explanation for the sensitivity of IL5 to protein synthesis inhibitors and a mechanism for the specific induction of IL5 compared with other cytokines.

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