死体亡途径的细胞类型依赖性是由病毒感染引发的
Heather Koehler1,2,3, Derek Titus3,4, Crystal Lawson1,2,3
1School of Molecular Biosciences and Center for Reproductive Biology, Washington State University, Pullman, WA, USA.
The FEBS journal
|December 25, 2023
概括
细胞亡是一种编程细胞死亡,它使用Z-DNA结合蛋白1 (ZBP1) 或瘤亡因子 (TNF) 途径来对抗病毒. 细胞类型决定了哪种亡途径是主导的,从而影响宿主对感染的防御.
科学领域:
- 免疫学 免疫学 免疫学
- 细胞生物学 细胞生物学
- 病毒学 病毒学
背景情况:
- 亡是对抗病毒感染的关键宿主防御机制.
- 三种途径启动亡:收费类受体3 (TLR3) -TIR域含有适应器诱导的干扰素-β (TRIF),Z-DNA结合蛋白1 (ZBP1) 和瘤亡因子 (TNF) α.
- ZBP1和TNF通路是控制病毒感染的关键,而TLR3-TRIF的作用是不太了解的.
研究的目的:
- 在病毒感染期间调查ZBP1介导和TNF介导的亡途径的不同作用和细胞类型特定激活.
- 了解病毒如何逃避宿主防御机制,以及工程病毒如何触发特定的亡途径.
主要方法:
- 利用缺乏编程细胞死亡病毒抑制剂的工程病毒 (小鼠细胞巨乳病毒M45mutRHIM和疫苗病毒E3∆Zα).
- 感染的小鼠胚胎纤维细胞和骨髓衍生的巨细胞与工程病毒.
- 使用RIPK1抑制剂或TNF阻断来评估通路优势的阻断TNF信号传递.
主要成果:
- 工程病毒在小鼠胚胎纤维细胞中触发了ZBP1-依赖性亡.
- 在骨髓衍生的巨细胞中,亡主要通过TNF介导的途径启动.
- 阻断TNF通路将亡的启动转移到巨细胞中的ZBP1-介导通路.
结论:
- 宿主细胞在对病毒感染的反应中表现出对TNF介导或ZBP1介导的亡途径的偏好.
- 这些细胞类型的特定偏好对于理解宿主病毒相互作用和开发准确的疾病模型至关重要.
- 考虑这些路径偏好对于评估炎症和病毒控制的平衡 in vivo 是必不可少的.
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