炎症记忆使皮肤上皮干细胞对组织损伤敏感
Shruti Naik1, Samantha B Larsen1, Nicholas C Gomez1
1Robin Chemers Neustein Laboratory of Mammalian Cell Biology and Development, Howard Hughes Medical Institute, The Rockefeller University, New York, New York 10065, USA.
Nature
|October 19, 2017
概括
皮肤干细胞形成炎症记忆,加速受伤后的修复障碍. 这种由Aim2炎症酶激活驱动的适应性提高了反应能力,但可能会增加癌症风险.
科学领域:
- 免疫学
- 干细胞生物学
- 皮肤病学
背景情况:
- 皮肤屏障对防御至关重要,由上皮干细胞 (EpSC) 维持.
- 没有完全了解 EpSC 对炎症的反应及其长期影响.
- 这些细胞易受炎症损伤.
研究的目的:
- 研究急性炎症对小鼠上皮干细胞 (EpSC) 的持久后果.
- 确定 EpSC 适应和"记住"炎症事件的机制.
- 了解这种干细胞记忆如何影响皮肤屏障的修复.
主要方法:
- 在小鼠中的急性炎症模型.
- 在炎症后分析 EpSC 功能和基因表达.
- 有关Aim2,caspase-1和interleukin-1β的基因操纵.
主要成果:
- 鼠标EPSC表现出对急性炎症的长期记忆,加速二次损伤后的屏障恢复.
- 在 EpSC 中,这种功能性适应独立于皮肤固体巨细胞和T细胞.
- 在应激反应基因上保持染色体可访问性,在再次暴露于炎症时实现快速转录,由Aim2炎症体信号传递介导.
- 失去了Aim2,caspase-1或interleukin-1β会在EPSC中取消这种炎症记忆.
结论:
- 皮质干细胞具有内在的炎症记忆, 增强组织修复.
- 在建立和维持这种EPSC炎症记忆方面,Aim2炎症酶途径至关重要.
- 虽然对修复有好处,但由于炎症而增加的EPSC敏感性可能会增加对自身免疫性疾病和癌症的易感性.
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