微生物群调节TET1介导的DNA基甲基化程序在先天性淋巴细胞分化中
Xusheng Zhang1,2, Xintong Gao1,2, Zhen Liu1,2
1CAS Key Laboratory of Pathogen Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences, 100101, Beijing, China.
Nature communications
|June 5, 2024
概括
肠道微生物群通过通过TET1.1调节DNA甲基化来影响先天性淋巴细胞 (ILC) 的分化. 这种表观遗传重编程会影响ILC1的发育和肠道平衡.
科学领域:
- 免疫学 免疫学 免疫学
- 表观遗传学 在表观遗传学中,表观遗传学是指表观遗传学.
- 微生物学 微生物学
背景情况:
- 天生的淋巴细胞 (ILC) 对于免疫反应至关重要.
- 控制ILC与前体 (ILCP) 差异化的表观遗传机制尚未完全理解.
研究的目的:
- 在ILC分化过程中调查全基因组DNA甲基化和基甲基化动态.
- 阐明TET1在ILC子集规范中的作用以及肠道微生物群对这一过程的影响.
主要方法:
- 在ILC子集和前体中进行全基因组DNA甲基化和基甲基化分析.
- 使用遗传模型分析ILC差异化中的TET1功能.
- 研究微生物群诱导的TET1表达和表观遗传修饰的变化.
主要成果:
- TET1抑制了ILC1的分化,而它的缺乏通过抑制TGF-β信号来促进它.
- 在产后ILCP分化过程中,肠道微生物群降低了TET1水平,导致ILC1扩张.
- 在成年小鼠中,TET1通过抑制ILC1过激活来维持肠道平衡.
结论:
- 肠道微生物群通过TET1介导的DNA基甲基化对ILC差异化进行表观遗传编程.
- 这项研究揭示了微生物群,DNA甲基化和ILC发育之间的交叉声,影响了免疫平衡.
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