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

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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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