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Blood, 1 December 2005, Vol. 106, No. 12, pp. 3888-3894. Prepublished online as a Blood First Edition Paper on August 16, 2005; DOI 10.1182/blood-2004-12-4709. This Article Full Text Full Text (PDF) All Versions of this Article: 2004-12-4709v1 106/12/3888    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Appel, S. Articles by Brossart, P. Search for Related Content PubMed PubMed Citation Articles by Appel, S. Articles by Brossart, P. Related Collections Immunobiology Signal Transduction Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY PPAR- agonists inhibit toll-like receptor-mediated activation of dendritic cells via the MAP kinase and NF-B pathways Silke Appel, Valdete Mirakaj, Anita Bringmann, Markus M. Weck, Frank Grünebach, and Peter Brossart From the Department of Hematology, Oncology and Immunology, University of Tübingen, Tübingen, Germany. Dendritic cells (DCs) play an important role in initiating and maintaining primary immune responses. However, mechanisms involved in the resolution of these responses are elusive. We analyzed the effects of 15d-PGJ2 and the synthetic peroxisome proliferator-activated receptor (PPAR)- ligand troglitazone (TGZ) on the immunogenicity of human monocyte-derived DCs upon stimulation with toll-like receptor (TLR) ligands. Activation of PPAR- resulted in a reduced stimulation of DCs via the TLR ligands 2, 3, 4, and 7, characterized by down-regulation of costimulatory and adhesion molecules and reduced secretion of cytokines and chemokines involved in T-lymphocyte activation and recruitment. MCP-1 (monocyte chemotactic protein-1) production was increased due to PPAR- activation. Furthermore, TGZ-treated DCs showed a significantly reduced capacity to stimulate T-cell proliferation, emphasizing the inhibitory effect of PPAR- activation on TLR-induced DC maturation. Western blot analyses revealed that these inhibitory effects on TLR-induced DC activation were mediated via inhibition of the NF-B and mitogen-activated protein (MAP) kinase pathways while not affecting the PI3 kinase/Akt signaling. Our data demonstrate that inhibition of the MAP kinase and NF-B pathways is critically involved in the regulation of TLR and PPAR--mediated signaling in DCs. 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