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在小鼠中通过肠道EpCAM+DCIR2+cDC2s的IL-23表达获得了网红酸许可的Notch2
Daiya Ohara1, Yusuke Takeuchi1, Hitomi Watanabe1
1Laboratory of Integrative Biological Science, Institute for Life and Medical Sciences, Kyoto University , Kyoto, Japan.
The Journal of experimental medicine
|January 5, 2024
概括
研究人员确定了肠道中的特定免疫细胞,这些免疫细胞产生了介质蛋白-23 (IL-23). 在感染期间,Notch2和视网酸信号传递是开发这些IL-23产生细胞的关键.
科学领域:
- 免疫学 免疫学 免疫学
- 细胞生物学 细胞生物学
- 胃肠病学 胃肠病学
背景情况:
- 介素-23 (IL-23) 在粘膜免疫和炎症性疾病中起着关键作用.
- 细胞来源和IL-23产生细胞的发育调节尚未得到充分理解.
研究的目的:
- 研究肠道IL-23产生细胞的发育特征和调节.
- 阐明控制这些细胞分化的信号通路.
主要方法:
- 使用了一个Il23aVenus记者鼠标模型.
- 用鞭毛素刺激的细胞,并感染了Citrobacter rodentium.
- 通过流式细胞计量分析细胞种群,并描述信号通路.
主要成果:
- 确定了EpCAM+ DCIR2+ CD103-cDC2s作为肠关联淋巴组织中主要的IL-23生产者,称为cDCIL23.
- 已经证明,鞭毛素刺激或C. rodentium感染会诱导cDCIL23.
- 显示的Notch2信号对于cDC2发育至关重要,并结合Notch2和视网酸信号驱动终端分化成cDCIL23.
结论:
- 为肠道cDCIL23.23的发展建立了一个两步模式.
- 提供了关于IL-23-产生cDC2s在恒温和感染期间细胞动态和发育途径的见解.
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