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Originally published In Press as doi:10.1074/jbc.M101592200 on October 30, 2001

J. Biol. Chem., Vol. 276, Issue 52, 48871-48878, December 28, 2001
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Yin-Yang 1 Activates Interleukin-4 Gene Expression in T Cells*

Jia GuoDagger , Vincenzo Casolaro§, Edward Seto, Wen-Ming Yang, Cindy ChangDagger , Maria-Cristina Seminario§||, Judith KeenDagger , and Steve N. GeorasDagger §**

From the Divisions of Dagger  Pulmonary and Critical Care Medicine and § Allergy and Clinical Immunology, The Johns Hopkins Asthma and Allergy Center, Baltimore, Maryland 21224 and the  H. Lee Moffit Cancer Center and Research Institute, University of South Florida, Tampa, Florida 33612

Interleukin-4 (IL-4) is a multifunctional cytokine that plays an important role in immune and inflammatory responses. Expression of the IL-4 gene is tightly controlled at the level of gene transcription by both positive and negative regulatory elements in the IL-4 promoter. Several constitutive nuclear factors have been identified that can interact with IL-4 promoter elements in DNA binding assays. Here we report that the zinc-finger protein YY-1 (Yin-Yang 1) can bind to multiple elements within the human IL-4 promoter. Cotransfection of Jurkat T cells with different IL-4 promoter/reporter constructs together with expression vectors encoding antisense, wild-type, or zinc finger-deleted mutant YY-1 suggested that YY-1 enhanced IL-4 promoter activity in a DNA-binding domain-dependent manner. Site-directed mutagenesis revealed that a proximal YY-1-binding site, termed Y0 (-59TCATTTT-53), was essential for YY-1-driven IL-4 promoter activity. In addition, cotransfected YY-1 enhanced both IL-4 promoter activity and endogenous IL-4 gene expression in nontransformed peripheral blood T cells. Thus, YY-1 positively regulates IL-4 gene expression in lymphocytes.

* This work was supported by NHLBI Grant HLAI61875 from the National Institutes of Health and by research grants from the American Lung Association, the American Heart Association, and the Johns Hopkins University School of Medicine Clinician Scientist Program.The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

|| Present address: Laboratory of Cellular and Molecular Biology, NIA, NIH, Baltimore, MD 21224.

** To whom correspondence should be addressed: Johns Hopkins Asthma and Allergy Center, Rm. 4B.41, 5501 Hopkins Bayview Circle, Baltimore, MD 21224. Tel.: 410-550-2518; Fax: 410-550-2612; E-mail: sgeoras@jhmi.edu.

Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.


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