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Immunity. 2003 Sep;19(3):329-39.

PPARgamma promotes mannose receptor gene expression in murine macrophages and contributes to the induction of this receptor by IL-13.

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Laboratoire des Macrophages, Médiateurs de l'Inflammation et Interactions Cellulaires, Université Paul Sabatier--EA 2405, Institut National de la Santé et de la Recherche Médicale IFR 31, Hôpital Rangueil, 31403 Toulouse Cedex 4, France.


Macrophage mannose receptor (MMR) is an important component of the innate immune system implicated in host defense against microbial infections such as candidiasis and in antigen presentation. We demonstrate here that the MMR expression is induced in mouse peritoneal macrophages following exposure to PPARgamma ligands or to interleukine-13 (IL-13) via a PPARgamma signaling pathway. Ligand activation of the PPARgamma in macrophages promotes uptake, killing of Candida albicans, and reactive oxygen intermediates production triggered by the yeasts through MMR overexpression. We also show that MMR induction by IL-13 via PPARgamma is dependent on phopholipase A2 activation and that IL-13 induces 15d-PGJ2 production and nuclear localization. These results reveal a novel signaling pathway controlling the MMR surface expression and suggest that endogenous PPARgamma ligand produced by phospholipase A2 activation may be an important regulator of MMR expression by IL-13.

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