细胞衍生IL-25调节肠道ILC2上皮反应回路
Jakob von Moltke1, Ming Ji1,2, Hong-Erh Liang1
1Department of Medicine, University of California San Francisco, San Francisco, California 94143-0795, USA.
Nature
|December 18, 2015
概括
小肠中的细胞分泌IL-25,维持2组先天性淋巴细胞 (ILC2). 在虫感染时,这种相互作用驱动了上皮的重塑和粘液的产生,这对2型免疫至关重要.
科学领域:
- 免疫学
- 胃肠病学
- 细胞生物学
背景情况:
- 由寄生虫和过敏原引发的2型免疫反应涉及粘液的产生和光滑肌肉的收缩.
- 来自第2组先天性淋巴细胞 (ILC2s) 和T辅助细胞 (TH2细胞) 的互白素-13 (IL-13) 调节这些生理变化.
- 已知像IL-33,TSLP和IL-25这样的上皮细胞因子会激活ILC2,但它们的确切起源和调节尚未完全理解.
研究的目的:
- 研究小肠细胞在2型免疫中的作用.
- 阐明激活ILC2s的表皮信号的来源和调节.
- 在2型免疫反应中定义细胞循环介导表皮重塑.
主要方法:
- 虫感染的小鼠模型.
- 在肠上皮细胞和ILC2中分析基因表达和细胞因子的产生.
- 细胞系的追踪和功能测试.
主要成果:
- 细胞构成性地表达IL-25,在静止状态下维持ILC2平衡.
- 虫感染会增加细胞IL-25的产生,进一步激活ILC2s.
- 激活的ILC2s分泌IL-13,促进和杯细胞与上皮细胞的分化.
结论:
- 细胞,ILC2s和上皮原生细胞在2型免疫中形成肠上皮重塑的关键电路.
- 细胞衍生的IL-25对于维持ILC2s和调节"哭泣和扫荡"反应至关重要.
- 这一电路突出显示了宿主在粘膜屏障上的协调机制.
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