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J. Biol. Chem., Vol. 281, Issue 28, 19188-19195, July 14, 2006

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Interferon Regulatory Factor 8 Regulates RANTES Gene Transcription in Cooperation with Interferon Regulatory Factor-1, NF-B, and PU.1^*

From the Department of Microbiology and Immunology, Weill Medical College of Cornell University, New York, New York 10021

Interferon regulatory factor (IRF)-8 is a member of the IRF family of transcription factors important in interferon--mediated signaling and in the development and function of dendritic cells. Regulated on activation, normal T cell expressed and secreted (RANTES, or CCL5) is a member of the CC chemokine family of proteins, strongly chemoattractant for several important immune cell types in host defense against infectious agents and cancer. Here we report that RANTES expression in IRF-8-null macrophages stimulated with interferon- and lipopolysaccharide is markedly decreased. IRF-8 can activate RANTES gene transcription in synergism with IRF-1. Interestingly, IRF-8 can activate RANTES transcription independently of IRF-1 through direct physical interactions with NF-B c-Rel and PU.1 via the NF-B element located at –88 to –79 in vitro and in vivo. This study uncovers a novel role of IRF-8 in the regulation of RANTES gene expression and the underlying molecular mechanisms whereby IRF-8 interacts with several other important transcription factors to initiate innate immune responses to pathogenic and inflammatory challenges by activating the RANTES gene.

Received for publication, March 3, 2006 , and in revised form, May 4, 2006.

^* This work was supported by National Institutes of Health Grant CA100223 (to X. M.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ To whom correspondence should be addressed: Dept. of Microbiology and Immunology, Weill Medical College of Cornell University, 1300 York Ave., New York, New York 10021. Tel.: 212-746-4404; Fax: 212-746-4427; E-mail: xim2002{at}med.cornell.edu.

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