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J. Biol. Chem., Vol. 276, Issue 51, 48502-48509, December 21, 2001
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From the Interleukin-5 (IL-5) is a T-cell cytokine
involved in Type 2 diseases and is commonly described as being
coordinately regulated with other Type 2 cytokines, such as IL-4 and
IL-13. Considering the unique control of eosinophilia by IL-5, such
coordinate regulation would be surprising. In fact, the biological
specificity of eosinophilia and its control by IL-5 suggests a unique
and independent control of IL-5 regulation. In this report we show the
binding of GATA-3 to three sites in the human IL-5 promoter in
the human T-cell line PER117. The previously identified Department of Molecular Immunology, Curtin
University of Technology, and the Western Australian Institute of
Medical Research Level 5, Medical Research Foundation Building, Rear 50 Murray Street, Perth 6000, Western Australia, ¶ Institut Francais
des Boissons de la Brasserie et de la Malterie, Laboratoire de Biologie
Moleculaire, 7, rue du Bois de la Champelle, F-54500 Vandoeuvre,
France, and the Universite Libre de Bruxelles, Faculte de
Medecine, Laboratoire d'Immunologie Experimentale, CP615, 808 route de
Lennik, B1070 Brussels, Belgium
70 site and
another site at position 152 are shown to positively regulate IL-5
transcription. More importantly, the site located at 400 acts as a
powerful repressor of IL-5 transcription with mutagenesis of this site allowing a high level expression of IL-5 without the activation of
other factors normally required for IL-5 expression. Whereas GATA-3 has
been proposed to be involved in the regulation of the IL-4/IL-5/IL-13
locus, we show here that it has another function in controlling IL-5
transcription that supports the observed unique biological function of
this cytokine.
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