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Molecular and Cellular Biology, July 2004, p. 6488-6500, Vol. 24, No. 14
0270-7306/04/$08.00+0     DOI: 10.1128/MCB.24.14.6488-6500.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

The IB Kinase Complex and NF-B Act as Master Regulators of Lipopolysaccharide-Induced Gene Expression and Control Subordinate Activation of AP-1

Daniel Krappmann,^1* Elmar Wegener,¹ Yoshiaki Sunami,¹ Meral Esen,² Andreas Thiel,² Benjamin Mordmuller,^1, and Claus Scheidereit¹

Max Delbrück Center for Molecular Medicine, D-13122 Berlin,¹ Deutsches Rheuma-Forschungszentrum Berlin, 10117 Berlin,Germany²

Received 4 March 2004/ Accepted 21 April 2004

Toll-like receptors (TLRs) recognize conserved products of microbial pathogens to initiate the innate immune response. TLR4 signaling is triggered upon binding of lipopolysaccharides (LPS) from gram-negative bacteria. Using comparative gene expression profiling, we demonstrate a master regulatory role of IB kinase (IKK)/NF-B signaling for immediate-early gene induction after LPS engagement in precursor B cells. IKK/NF-B signaling controls a large panel of gene products associated with signaling and transcriptional activation and repression. Intriguingly, the induction of AP-1 activity by LPS in precursor B cells and primary dendritic cells fully depends on the IKK/NF-B pathway, which promotes expression of several AP-1 family members, including JunB, JunD, and B-ATF. In pre-B cells, AP-1 augments induction of a subset of primary NF-B targets, as shown for chemokine receptor 7 (CCR7) and immunoglobulin light chain. Thus, our data illustrate that NF-B orchestrates immediate-early effects of LPS signaling and controls secondary AP-1 activation to mount an appropriate biological response.

Present address: Department of Parasitology, University of Tübingen, 72074 Tübingen, Germany.

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