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内体自身RNARmrp参与TLR3二分化到原始先天激活的分子特征

Shikun Zhang¹, Bo Li², Lun Liu¹

¹Department of Immunology, Center for Immunotherapy, Institute of Basic Medical Sciences, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing, China.

|September 7, 2025

概括

自我RNA Rmrp在内分泌体中与托尔类受体3 (TLR3) 结合,诱导因天生的免疫激活的二分化. 这种对抗病毒反应至关重要的相互作用是由内体的pH调节的.

科学领域:

免疫学免疫学免疫学
结构生物学结构生物学
分子生物学分子生物学

背景情况:

收费类受体3 (TLR3) 分化对于天生的免疫识别至关重要.
对于TLR3预二分化和激活原始化的精确机制,人们仍然不完全理解.

研究的目的:

阐明自我RNA诱导的TLR3二分化和激活的机制.
确定自身RNARmrp和TLR3.3之间的相互作用的结构基础.

主要方法:

低温电子显微镜 (Cryo-EM) 用于确定Rmrp-TLR3复合物的结构.
在体外测试以评估TLR3二分化和结合.
在体内研究使用髓状细胞特异性Rmrp缺乏模型.

主要成果:

内基因局部化自我RNA Rmrp直接结合并诱导TLR3二分化,形成一种新的拉皮形状.
在这种相互作用中,Rmrp的3'-end和TLR3的K42残留物的特定结构特征至关重要.
在内体酸化后的Rmrp解离使TLR3二聚体成熟以激活.
骨髓细胞中Rmrp的缺乏会损害TLR3的二分化,并减弱抗病毒反应.

结论:

自我RNA Rmrp在早期内体内作为TLR3二分化的特定激活剂.
内体酸化调节Rmrp的解离,为TLR3进行先天的识别.
这项研究揭示了通过自身RNA激活TLR的新机制,并突出了细胞下RNA局部化在天生的免疫力中的作用.

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