过氧化物酶体增殖物激活受体γ（PPARγ）的激活可将人类单核细胞诱导分化为具有抗炎特性的替代性M2巨噬细胞。
PPARgamma activation primes human monocytes into alternative M2 macrophages with anti-inflammatory properties.
作者信息
Bouhlel M Amine, Derudas Bruno, Rigamonti Elena, Dièvart Rébecca, Brozek John, Haulon Stéphan, Zawadzki Christophe, Jude Brigitte, Torpier Gérard, Marx Nikolaus, Staels Bart, Chinetti-Gbaguidi Giulia
机构信息
Institut Pasteur de Lille, F-59019 Lille, France; Inserm, U545, F-59019 Lille, France.
出版信息
Cell Metab. 2007 Aug;6(2):137-43. doi: 10.1016/j.cmet.2007.06.010.
Th1 cytokines promote monocyte differentiation into proatherogenic M1 macrophages, while Th2 cytokines lead to an "alternative" anti-inflammatory M2 macrophage phenotype. Here we show that in human atherosclerotic lesions, the expression of M2 markers and PPARgamma, a nuclear receptor controlling macrophage inflammation, correlate positively. Moreover, PPARgamma activation primes primary human monocytes into M2 differentiation, resulting in a more pronounced anti-inflammatory activity in M1 macrophages. However, PPARgamma activation does not influence M2 marker expression in resting or M1 macrophages, nor does PPARgamma agonist treatment influence the expression of M2 markers in atherosclerotic lesions, indicating that only native monocytes can be primed by PPARgamma activation to an enhanced M2 phenotype. Furthermore, PPARgamma activation significantly increases expression of the M2 marker MR in circulating peripheral blood mononuclear cells. These data demonstrate that PPARgamma activation skews human monocytes toward an anti-inflammatory M2 phenotype.
Th1细胞因子促进单核细胞分化为促动脉粥样硬化的M1巨噬细胞，而Th2细胞因子则导致“替代性”抗炎M2巨噬细胞表型。我们在此表明，在人类动脉粥样硬化病变中，M2标志物的表达与PPARγ（一种控制巨噬细胞炎症的核受体）呈正相关。此外，PPARγ激活使原代人单核细胞向M2分化，导致M1巨噬细胞中抗炎活性更显著。然而，PPARγ激活并不影响静息或M1巨噬细胞中M2标志物的表达，PPARγ激动剂治疗也不影响动脉粥样硬化病变中M2标志物的表达，这表明只有天然单核细胞可通过PPARγ激活被诱导为增强的M2表型。此外，PPARγ激活显著增加循环外周血单个核细胞中M2标志物MR的表达。这些数据表明，PPARγ激活使人类单核细胞向抗炎M2表型倾斜。
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