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通过依赖于LKB1的方式调节ILC2铁,α-Tocopherol可以改善过敏呼吸道炎症

Xiaogang Zhang¹, Jingping Liu², Ziyang Chen³

¹Pediatric Intensive Care Unit, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences); Department of Immunology, School of Basic Medical Sciences; Department of Clinical Laboratory, the Third Affiliated Hospital of Southern Medical University, Southern Medical University, Guangzhou 510515, China; Department of Immunology, School of Basic Medical Sciences; Guangdong Provincial Key Laboratory of Single-cell and Extracellular Vesicles, Southern Medical University, Guangzhou 510515, China.

Molecular therapy : the journal of the American Society of Gene Therapy

|September 3, 2025

概括

维生素E成分α-托科菲罗尔 (α-Toc) 通过抑制2组先天性淋巴细胞 (ILC2) 中的B类清除受体1 (SCARB1) 和LKB1-AMPK/mTOR通路来调节过敏呼吸道炎症. 这表明α-Toc是一种潜在的喘治疗方法.

科学领域:

免疫学
细胞生物学
营养科学

背景情况:

饮食免疫可以调节过敏的呼吸道炎症.
2组先天性淋巴细胞 (ILC2) 是过敏气道炎症的关键媒介.

研究的目的:

确定调节ILC2介导的过敏呼吸道炎症的饮食成分.
阐明alpha-tocopherol (α-Toc) 对ILC2s和过敏呼吸道炎症的影响的分子机制.

主要方法:

接受α-Toc治疗的小鼠肺部ILC2s的转录组分析.
使用基因缺陷或关键路径的药理抑制的小鼠进行体内研究 (LKB1,SCARB1).
人类ILC2s的ex vivo培养以评估α-Toc的作用.

主要成果:

α-Toc治疗降低了SCARB1的表达,并抑制了肺部ILC2中的LKB1-AMPK/ mTOR通路.
缺乏LKB1或SCARB1对抗性导致ILC2的丰度,功能和肺炎的降低.
在LKB1缺乏的小鼠中,α-Toc未能改善炎症,这表明LKB1的关键作用.
通过调节KLF4-GPX4复合体,LKB1缺乏促进了ILC2s中的铁亡,减少了肺炎.
在人体ILC2中,α-Toc抑制了ILC2激活和LKB1介导的铁.

结论:

通过向LKB1-AMPK/mTOR通路并促进ILC2铁亡,α-Toc作为过敏气道炎症的饮食调节剂.
ILC2s中的LKB1介导铁是过敏呼吸道炎症的关键机制.
由于它能够抑制ILC2激活和铁死,α-Toc显示出治疗喘的潜力.

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