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J. Biol. Chem., Vol. 279, Issue 53, 55176-55186, December 31, 2004
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From the Department of Biological Sciences, Rutgers University, Newark, New Jersey 07102
In response to pathogen-associated molecular patterns, dendritic cells initiate an innate immune response characterized by expression and release of proinflammatory cytokines and chemokines. The extent of the inflammatory response is limited by various endogenous factors, including lipid mediators such as prostaglandin E2 (PGE2). We described previously the inhibitory effect of PGE2 on the expression and release of the inflammatory chemokines CCL3 and CCL4 from activated dendritic cells. In this study we describe a novel PGE2 signaling pathway that proceeds through EP-2 
cAMP EPAC phosphatidylinositol 3-kinase protein kinase B GSK-3 and results in increased DNA binding of the CCAAT displacement protein (CDP), a potent mammalian transcriptional repressor. The direct link between CDP and CCL3/4 transcription was established in knock-down experiments using CDP small interference RNA.
Received for publication, August 26, 2004 , and in revised form, September 27, 2004.
* This work was supported by National Institutes of Health Grants AI47325 and AI52306 (to D. G.) and the Johnson & Johnson Neuroimmunology Fellowships (to H. J.). 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.
To whom correspondence should be addressed: Dept. of Biological Sciences, Rutgers University, 101 Warren St., Newark, NJ 07102. Tel.: 973-353-1162; Fax: 973-353-1007; E-mail: dganea{at}andromeda.rutgers.edu.
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