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机械激活的纤维细胞促进肺组2的先天性淋巴细胞可塑性,推动病的进展

Yangyang He^1,2,3, Fan Yang^1,2, Lin Yang^1,2

¹Key Laboratory of Environmental Stress and Chronic Disease Control & Prevention (China Medical University), Ministry of Education, Shenyang, Liaoning, PR China.

Nature communications

|November 12, 2024

概括

激活的纤维细胞通过通过Notch3-IL-18通路改变免疫细胞来驱动病的进展. 这项研究揭示了肺纤维化的新治疗点.

科学领域:

免疫学免疫学免疫学
细胞生物学细胞生物学
肺部医学肺部医学

背景情况:

暴露在晶体二氧化 (CS) 中会导致,一种渐进的肺纤维化.
纤维细胞是纤维生成的关键,但它们在病中的免疫作用尚不清楚.
在病的进展过程中,2组先天性淋巴细胞 (ILC2) 转化为ILC1.

研究的目的:

研究纤维细胞在CS诱导的肺纤维化中的免疫调节作用.
阐明纤维细胞通过哪些机制影响着病中的免疫细胞动态.
为了确定病和其他纤维性肺部疾病的潜在治疗点.

主要方法:

使用了一种CS诱导的肺纤维化小鼠模型.
研究了纤维细胞激活及其对免疫细胞群,特别是ILCs的影响.
研究了Notch3信号传递和INTERLEUKIN-18 (IL-18) 在纤维细胞介导免疫反应中的作用.
在纤维细胞中进行了Notch3淘汰,以评估其对纤维化和ILC转化的影响.

主要成果:

激活的纤维细胞在化中调解ILC2s转化为ILC1s.
这种ILC转化受纤维细胞衍生IL-18.8的调节.
在激活的纤维细胞中,Notch3信号控制了通过caspase 1控制IL-18的产生.
纤维细胞特异性Notch3淘汰减弱性肺纤维化和小鼠中的ILC转化.

结论:

激活的纤维细胞是化过程中ILC2-ILC1转换的关键调节者.
纤维细胞中的Notch3-IL-18信号轴对于病的进展至关重要.
向纤维细胞介导免疫调节为肺纤维化疾病提供了潜在的治疗策略.

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