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Jmjd3-Irf4 轴调节 M2 巨噬细胞极化和宿主对寄生虫感染的反应。

The Jmjd3-Irf4 axis regulates M2 macrophage polarization and host responses against helminth infection.

机构信息

Laboratory of Host Defense, World Premiere Initiative Immunology Frontier Research Center, Osaka University, Osaka, Japan.

出版信息

Nat Immunol. 2010 Oct;11(10):936-44. doi: 10.1038/ni.1920. Epub 2010 Aug 22.

Abstract

Polarization of macrophages to M1 or M2 cells is important for mounting responses against bacterial and helminth infections, respectively. Jumonji domain containing-3 (Jmjd3), a histone 3 Lys27 (H3K27) demethylase, has been implicated in the activation of macrophages. Here we show that Jmjd3 is essential for M2 macrophage polarization in response to helminth infection and chitin, though Jmjd3 is dispensable for M1 responses. Furthermore, Jmjd3 (also known as Kdm6b) is essential for proper bone marrow macrophage differentiation, and this function depends on demethylase activity of Jmjd3. Jmjd3 deficiency affected trimethylation of H3K27 in only a limited number of genes. Among them, we identified Irf4 as encoding a key transcription factor that controls M2 macrophage polarization. Collectively, these results show that Jmjd3-mediated H3K27 demethylation is crucial for regulating M2 macrophage development leading to anti-helminth host responses.

摘要

巨噬细胞向 M1 或 M2 细胞的极化对于针对细菌和寄生虫感染的反应至关重要。包含 Jumonji 结构域的 3(Jmjd3)是一种组蛋白 3 赖氨酸 27(H3K27)去甲基酶,它参与了巨噬细胞的激活。在这里,我们表明 Jmjd3 对于寄生虫感染和几丁质诱导的 M2 巨噬细胞极化是必不可少的,尽管 Jmjd3 对于 M1 反应是可有可无的。此外,Jmjd3(也称为 Kdm6b)对于骨髓巨噬细胞的正常分化是必不可少的,并且这个功能依赖于 Jmjd3 的去甲基酶活性。Jmjd3 缺乏仅影响了少数几个基因的 H3K27 三甲基化。其中,我们鉴定出 Irf4 编码一种关键的转录因子,它控制 M2 巨噬细胞极化。总之,这些结果表明 Jmjd3 介导的 H3K27 去甲基化对于调节 M2 巨噬细胞的发育至关重要,从而导致抗寄生虫宿主反应。

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