ILC3s通过STING感知肠道微生物群,以启动免疫耐受性
Wenqing Zhou1, Jordan Z Zhou1, Anees Ahmed1
1Joan and Sanford I. Weill Department of Medicine, Division of Gastroenterology and Hepatology, Weill Cornell Medicine, Cornell University, New York, NY, USA; Department of Microbiology & Immunology, Weill Cornell Medicine, Cornell University, New York, NY, USA; Jill Roberts Institute for Research in Inflammatory Bowel Disease, Weill Cornell Medicine, Cornell University, New York, NY, USA.
Immunity
|June 17, 2025
概括
第三组先天性淋巴细胞 (ILC3) 通过STING信号传递感知肠道微生物,促进免疫耐受性. 然而,炎症期间过度激活STING会导致ILC3细胞死亡,阻碍保护性免疫力.
科学领域:
- 免疫学 免疫学 免疫学
- 微生物学 微生物学
- 细胞生物学 细胞生物学
背景情况:
- 对肠道微生物群的免疫耐受性对健康至关重要.
- 启动对肠道微生物免疫耐受性的机制尚未完全理解.
- 第三组先天性淋巴细胞 (ILC3s) 是肠道免疫的关键参与者.
研究的目的:
- 研究抗原呈现细胞在启动对肠道微生物群的免疫耐受性中的作用.
- 阐明在肠道微生物殖民和炎症期间ILC3s中STING信号的功能.
主要方法:
- 大肠中MHC II+细胞的单细胞分析.
- 通过病原生物Helicobacter hepaticus进行殖民.
- 分析ILC3s中的STING信号通路和细胞迁移.
主要成果:
- ILC3s作为RORγt+抗原呈现细胞,表达STING信号的功能.
- ILC3s中的STING信号使微生物能够感知并迁移到淋巴结.
- ILC3内在的STING信号传递促进调节性T细胞诱导,抑制炎症.
- 在肠道炎症期间,大量的STING激活会导致ILC3细胞死亡.
结论:
- 在ILC3s中,STING是肠道微生物群的关键传感器.
- 在稳定状态下,ILC3s中的STING信号促进免疫耐受性.
- 在炎症期间增加的STING激活是有害的,导致保护ILC3s的丧失.
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