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组织内在的IL-33/EGF电路在肠道受伤后促进上皮质再生
Marco Calafiore1,2, Ya-Yuan Fu1,2, Paola Vinci1,2
1Human Oncology & Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, NY, 10065, USA.
Nature communications
|September 5, 2023
概括
肠干细胞 (ISC) 使用Interleukin-33 (IL-33) 途径向Paneth细胞发出信号,然后产生表皮生长因子 (EGF) 以促进损伤后的肠道修复.
科学领域:
- 胃肠病学 胃肠病学
- 干细胞生物学 干细胞生物学
- 免疫学 免疫学 免疫学
背景情况:
- 肠干细胞 (ISC) 对于维持肠表皮至关重要.
- 管理ISC监管的机制及其在损害后的利基市场尚未完全理解.
- 介素-33 (IL-33) /ST2轴是免疫调节途径和肠道损伤的临床生物标志物.
研究的目的:
- 研究IL-33/ST2轴在辐射损伤后肠上皮质再生中的作用.
- 阐明涉及ISC的信号通路,它们的位和上皮质修复.
主要方法:
- 辐射伤害模型模拟肠道病理.
- 三维成像技术. 三维成像技术.
- 在干细胞区内诱导特定于血统的RiboTag.
主要成果:
- 在对辐射损伤的反应中,ISCs表达IL-33.
- 由IL-33刺激的帕内斯细胞增加了表皮生长因子 (EGF) 的产生.
- EGF促进ISC恢复和肠上皮再生.
结论:
- 确定了一条新的再生途径,该位在动态地对损伤做出反应.
- 通过IL-33/ST2/EGF轴,ISC通过调节其利基来协调再生.
- 这条途径在治疗肠道损伤方面具有治疗潜力,突出显示了IL-33在免疫调节之外的作用.
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