PPARγ promotes mannose receptor gene expression in murine macrophages and contributes to the induction of this receptor by IL-13
PPARγ promotes mannose receptor gene expression in murine macrophages and contributes to the induction of this receptor by IL-13
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DOI：
10.1016/s1074-7613(03)00229-2
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发表时间：
2003-09-01
期刊：
影响因子：
32.4
通讯作者：
Pipy, B
中科院分区：
文献类型：
--
作者：
Coste, A;Dubourdeau, M;Pipy, B
巨噬细胞甘露糖受体 (MMR) 是先天免疫系统的重要组成部分，涉及宿主防御念珠菌病等微生物感染和抗原呈递。我们在此证明，在暴露于 PPARgamma 配体或白细胞介素 13 (IL-13) 后，通过 PPARgamma 信号通路在小鼠腹膜巨噬细胞中诱导 MMR 表达。巨噬细胞中 PPARgamma 的配体激活可促进白色念珠菌的摄取和杀死，以及酵母菌通过 MMR 过度表达引发活性氧中间体的产生。我们还表明，IL-13 通过 PPARgamma 诱导 MMR 依赖于磷脂酶 A2 的激活，并且 IL-13 诱导 15d-PGJ2 的产生和核定位。这些结果揭示了控制 MMR 表面表达的新信号通路，并表明磷脂酶 A2 激活产生的内源性 PPARgamma 配体可能是 IL-13 对 MMR 表达的重要调节因子。
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.