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首页> 外文期刊>Cytokine >IL-10 is required for polarization of macrophages to M2-like phenotype by mycobacterial DnaK (heat shock protein 70)
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IL-10 is required for polarization of macrophages to M2-like phenotype by mycobacterial DnaK (heat shock protein 70)

机译：分枝杆菌DnaK（热激蛋白70）使巨噬细胞极化为M2样表型需要IL-10

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摘要

Macrophages are key cells in the innate immune system. They phagocytose pathogens and cellular debris, promote inflammation, and have important roles in tumor immunity. Depending on the microenvironment, macrophages can polarize to M1 (inflammatory) or M2 (anti-inflammatory) phenotypes. Extracellular DnaK (the bacterial ortholog of the mammalian Hsp70) from Mycobacterium tuberculosis (Mtb) was described to exert immune modulatory roles in an IL-10 dependent manner. We have previously observed that endotoxin-free DnaK can polarize macrophages to an M2-like phenotype. However, the mechanisms that underlie this polarization need to be further investigated. IL-10 has been described to promote macrophage polarization, so we investigated the involvement of this cytokine in macrophages stimulated with extracellular DnaK. IL-10 was required to induce the expression of M2 markers - Ym1 and Fizz, when macrophages were treated with DnaK. Blockade of IL-10R also impaired DnaK induced polarization, demonstrating the requirement of the IL-10/IL-10R signaling pathway in this polarization. DnaK was able to induce TGF-beta mRNA in treated macrophages in an IL-10 dependent manner. However, protein TGF-beta could not be detected in culture supernatants. Finally, using an in vivo allogeneic melanoma model, we observed that DnaK-treated macrophages can promote tumor growth in an 1-10-dependent manner. Our results indicate that the IL-10/IL-R axis is required for DnaK-induced M2-like polarization in murine macrophages. (C) 2016 Elsevier Ltd. All rights reserved.
机译：巨噬细胞是先天免疫系统中的关键细胞。它们吞噬细胞中的病原体和细胞碎片，促进炎症，并在肿瘤免疫中发挥重要作用。取决于微环境，巨噬细胞可以极化为M1（炎性）或M2（抗炎）表型。描述了来自结核分枝杆菌（Mtb）的细胞外DnaK（哺乳动物Hsp70的细菌直系同源物）以IL-10依赖的方式发挥免疫调节作用。我们以前已经观察到无内毒素的DnaK可以使巨噬细胞极化为M2样表型。但是，这种极化的基础机制需要进一步研究。已经描述了IL-10促进巨噬细胞极化，因此我们研究了这种细胞因子与细胞外DnaK刺激的巨噬细胞的关系。当用DnaK处理巨噬细胞时，需要IL-10诱导M2标记-Ym1和Fizz的表达。 IL-10R的阻滞也削弱了DnaK诱导的极化，表明在这种极化中需要IL-10 / IL-10R信号通路。 DnaK能够以IL-10依赖性方式在治疗的巨噬细胞中诱导TGF-βmRNA。但是，在培养上清液中未检测到TGF-β蛋白。最后，使用体内同种异体黑色素瘤模型，我们观察到DnaK处理的巨噬细胞可以以1-10依赖性方式促进肿瘤生长。我们的结果表明，IL-10 / IL-R轴是鼠巨噬细胞中DnaK诱导的M2样极化所必需的。 （C）2016 Elsevier Ltd.保留所有权利。

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