慢性炎症会永久地重塑细胞内免疫力
Toufic Mayassi1, Kristin Ladell2, Herman Gudjonson3
1Committee on Immunology, University of Chicago, Chicago, IL, USA; Department of Medicine, University of Chicago, Chicago, IL, USA.
Cell
|February 12, 2019
概括
在乳病 (CeD) 中,由质引起的慢性炎症会消耗特定的免疫细胞 (Vγ4+/Vδ1+ IEL). 这种肠道免疫的重新配置是永久的,即使在去除质后.
科学领域:
- 免疫学
- 胃肠病学
- 细胞生物学
背景情况:
- 组织常驻的淋巴细胞对于免疫监测至关重要.
- 这些细胞对慢性炎症的反应尚不清楚.
- 结核病为研究抗原驱动炎症提供了一个模型.
研究的目的:
- 研究质诱导的慢性炎症对结核病中的T细胞受体三角细胞 (TCRγδ+) 内皮细胞 (IELs) 的影响.
- 了解炎症和恢复期间IEL群体变化的分子机制.
主要方法:
- 在患者中分析Vγ4+/ Vδ1+IEL及其T细胞受体 (TCR).
- 在肠道中评估Butyrophilin-like (BTNL) 分子表达 (BTNL3/BTNL8).
- 在饮食中排除质后监测IEL群体和BTNL8表达.
主要成果:
- 在CeD中,质暴露导致了Vγ4+/Vδ1+IELs的显著耗尽,这些IELs识别了BTNL3/BTNL8.
- 一个具有减少BTNL8表达的新利基出现了,同时增加了具有明显TCR的质敏感Vδ1+IEL.
- 质取消恢复了BTNL8表达,但没有完全重建Vγ4+/ Vδ1+ IEL子集.
结论:
- 在CeD中,慢性质炎症会永久改变组织内存在的TCRγδ+ IEL区.
- 这项研究揭示了肠道免疫格局的持续重构.
- 这些发现凸显了慢性炎症对免疫细胞群的长期后果.
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