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Peroxisome proliferator‐activated receptor γ activators inhibit interleukin‐12 production in murine dendritic cells
Author(s) -
Faveeuw Christelle,
Fougeray Sylvie,
Angeli Véronique,
Fontaine Josette,
Chinetti Giulia,
Gosset Philippe,
Delerive Philippe,
Maliszewski Charlie,
Capron Monique,
Staels Bart,
Moser Muriel,
Trottein François
Publication year - 2000
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(00)02319-x
Subject(s) - peroxisome proliferator activated receptor , microbiology and biotechnology , receptor , activator (genetics) , nuclear receptor , biology , glucose homeostasis , cd40 , dendritic cell , immune system , chemistry , transcription factor , in vitro , endocrinology , immunology , biochemistry , cytotoxic t cell , insulin resistance , insulin , gene
Peroxisome proliferator‐activated receptors (PPARs) are members of the nuclear receptor superfamily. They are divided into three subtypes (α, β or δ, and γ) and are involved in lipid and glucose homeostasis and in the control of inflammation. In this study, we analyzed the expression of PPARs in murine dendritic cells (DCs), the most potent antigen presenting cells. We find that immature as well as mature spleen‐derived DCs express PPARγ, but not PPARα, mRNA and protein. We also show that the PPARγ activator rosiglitazone does not interfere with the maturation of DCs in vitro nor modifies their ability to activate naive T lymphocytes in vivo. Finally, we present evidence that PPARγ activators down‐modulate the CD40‐induced secretion of interleukin‐12, a potent Th1‐driving factor. These data suggest a possible role for PPARγ in the regulation of immune responses.