依赖于ED的组素修饰调节了iNKT细胞发育程序,缓解了肝损伤
Yun Guo1, Shun Ohki1, Yohei Kawano1
1Department of Immunology, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Frontiers in immunology
|October 7, 2024
概括
聚合体抑制复合体2 (PRC2) 在表观遗传上调节不变的自然杀手T (iNKT) 细胞发育. 删除Eed,一个PRC2子单元,严重减少iNKT细胞和增加肝损伤易感性.
科学领域:
- 表观遗传学 在表观遗传学中,表观遗传学是指表观遗传学.
- 免疫学 免疫学 免疫学
- 细胞生物学 细胞生物学
背景情况:
- 多镇压复合体2 (PRC2) 是一个关键的表观遗传调节器.
- 在PRC2中介于素H3氨酸27三甲基化 (H3K27me3).
- 在不变的自然杀手T (iNKT) 细胞发育中PRC2的作用尚未完全理解.
研究的目的:
- 研究PRC2在iNKT细胞发育和功能中的生理作用.
- 阐明iNKT细胞分化背后的表观遗传机制.
主要方法:
- 在小鼠T细胞中条件删除Eed,一个核心PRC2子单元.
- 流细胞计分析iNKT细胞种群.
- 基因表达分析和H3K27me3水平的评估.
主要成果:
- 缺少Eed导致iNKT细胞数量显著减少,特别是NKT1和NKT17子集.
- iNKT细胞分化受损,细胞死亡增加.
- 降低了H3K27me3水平,改变了Zbtb16,Cdkn2a和Cdkn1a的表达.
- 缺乏EED的小鼠对乙氨基诱导的肝损伤的敏感性增加.
结论:
- 以EED为媒介的H3K27me3对于iNKT细胞的发育,分化和生存至关重要.
- PRC2在维持肝脏内存的iNKT细胞的平衡中起着至关重要的作用.
- 通过PRC2进行表观遗传调节对于iNKT细胞特异性转录程序至关重要.
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