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TLR2 支持 γδ T 细胞 IL-17A 通过代谢重编程对眼睛表面同伴的反应

Wenjie Zhu^1,2, Xiaoyan Xu¹, Vijayaraj Nagarajan¹

¹Laboratory of Immunology, NEI, NIH Bethesda MD 20892, USA.

bioRxiv : the preprint server for biology

|May 7, 2024

概括

眼睛表面的共体微生物激活特定的T细胞. 在Vγ6 T细胞中内在的TLR2信号驱动了代谢变化和IL-17A的产生,这对粘膜免疫至关重要.

科学领域:

免疫学免疫学免疫学
微生物学微生物学
细胞生物学细胞生物学

背景情况:

眼睛表面的微生物调节局部免疫力.
像Corynebacterium mastitidis这样的共生细菌诱导结膜T细胞的保护性IL-17反应.

研究的目的:

为了确定结膜中的新型微生物响应T细胞子集.
阐明Vγ6 T细胞在应对*C. mastitidis*时的独特激活要求.

主要方法:

流细胞计和细胞因子分析以表征T细胞反应.
基因表达和表观遗传学分析,以了解分子机制.
在小鼠模型中研究 *in vivo* 免疫反应.

主要成果:

鉴定出Vγ6 T细胞是对*C. mastitidis*反应的主要亚群.
Vγ6细胞的最佳IL-17A产生需要外部 (树突细胞) 和内在的TLR2刺激.
内在的TLR2信号诱导表观遗传修饰和代谢转向脂肪酸氧化,支持IL-17A转录.
IκBζ被确定为TLR2上调的关键转录因子,对这一过程至关重要.

结论:

内在的TLR2信号传递对Vγ6T细胞功能至关重要.
在T细胞中微生物组诱导的代谢重编程支持IL-17A的产生.
这项研究揭示了一种由特定的 γδ T 细胞介导的粘膜免疫的新机制.

关键词:

粮农组织粮农组织粮农组织粮农组织.它们的IL-17A是IL-17A.眼睛的共量体.在TLR2中,它是TLR2.的 γδ T 细胞.

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