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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 (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 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. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted December 13, 2004 Accepted August 9, 2005 PPAR-gamma agonists inhibit toll-like receptor mediated activation of dendritic cells via the MAP kinase and NF-kappaB pathways Silke Appel, Valdete Mirakaj, Anita Bringmann, Markus M Weck, Frank Grunebach, and Peter Brossart* Department of Hematology, Oncology and Immunology, University of Tubingen, Tubingen, Germany * Corresponding author; email: peter.brossart{at}med.uni-tuebingen.de. Dendritic cells (DC) play an important role in initiating and maintaining of primary immune responses. However, mechanisms involved in the resolution of these responses are elusive. We analyzed the effects of 15d-PGJ2 and the synthetic PPAR-gamma ligand troglitazone (TGZ) on the immunogenicity of human monocyte derived DC upon stimulation with toll-like receptor (TLR) ligands. Activation of PPAR-gamma resulted in a reduced stimulation of DC via the TLR ligands 2, 3, 4 and 7, characterized by downregulation of costimulatory and adhesion molecules and reduced secretion of cytokines and chemokines involved in T lymphocyte activation and recruitment. MCP-1 production was increased due to PPAR-gamma activation. Furthermore, TGZ treated DC 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 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-gamma mediated signaling in DC. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? 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