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 Blood, 1 November 2007, Vol. 110, No. 9, pp. 3271-3280.
Prepublished online as a Blood First Edition Paper on July 30, 2007; DOI 10.1182/blood-2007-06-096222.

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IMMUNOBIOLOGY

PPAR{gamma} regulates the function of human dendritic cells primarily by altering lipid metabolism

Istvan Szatmari1, Daniel Töröcsik1, Maura Agostini2, Tibor Nagy3, Mark Gurnell2, Endre Barta3, Krishna Chatterjee2, and Laszlo Nagy1

1 Department of Biochemistry and Molecular Biology, Research Center for Molecular Medicine, University of Debrecen, Medical and Health Science Center, Debrecen, Hungary; 2 Department of Medicine, University of Cambridge, Cambridge, United Kingdom; and 3 Agricultural Biotechnology Center, Gödöllo, Hungary

Activation of the lipid-regulated nuclear receptor peroxisome proliferator-activated receptor gamma (PPAR{gamma}) modifies the immunophenotype of monocyte-derived dendritic cells (DCs). However it has not been analyzed in a systematic manner how lipid metabolism and immune regulation are connected at the transcriptional level via this receptor. Here we present the genome-wide expression analyses of PPAR{gamma}-instructed human DCs. Receptor activation was achieved by exogenous, synthetic as well as endogenous, natural means. More than 1000 transcripts are regulated during DC development by activation of PPAR{gamma}; half of the changes are positive effects. These changes appear to enhance and modulate the robust gene expression alterations associated with monocyte to DC transition. Strikingly, only genes related to lipid metabolism are overrepresented among early induced genes. As a net consequence, lipid accumulation appears to be diminished in these cells. In contrast, genes related to immune response are regulated after 24 hours, implying the existence of indirect mechanisms of modulation. Receptor dependence was established by using DCs of patients harboring a dominant-negative mutation of PPAR{gamma}. Our data show that PPAR{gamma} acts as a mostly positive transcriptional regulator in human developing DCs, acting primarily through controlling genes involved in lipid metabolism and via this, indirectly modifying the immune phenotype.


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Linking metabolism to immunity through PPAR{gamma}
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Blood 2007 110: 3092-3093. [Full Text] [PDF]



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