毒素效应体GRA15驱动的CCL5分泌增强了通过微血管封存细胞来增加大脑寄生虫负载
Elena Afanaseva1, Matias E Rodriguez1, Antonio Barragan1
1Department of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, Stockholm, Sweden.
mBio
|January 13, 2026
概括
毒素菌感染劫持宿主细胞以产生CCL5 (C-C动机连接体5),这是一个吸引免疫细胞进入大脑的分子. 阻止这种途径可以减少寄生虫的传播和大脑的殖民.
科学领域:
- 免疫学 免疫学 免疫学
- 神经科学是一个神经科学.
- 寄生虫学的寄生虫学
背景情况:
- 毒素菌通过利用宿主细胞进行系统传播.
- 寄生性细胞与大脑内皮相互作用的机制尚不清楚.
研究的目的:
- 研究T. gondii如何操纵大脑内皮细胞.
- 阐明C-C动态连接体5 (CCL5) 在T. gondii中枢神经系统传播中的作用.
主要方法:
- 主要的大脑内皮细胞和树突细胞 (DCs) 被T. gondii感染.
- 通过转录和分泌上调来分析CCL5诱导.
- 评估了寄生虫作用者GRA15和TEEGR的作用.
- 进行了受感染的DC迁移和转移测定.
- 用小鼠模型来研究CCL5上调和CCR5抗效应.
主要成果:
- T. gondii感染,而不是溶解物,通过GRA15和NF-κB信号传递在内皮细胞和DC中调节CCL5.
- 受感染的DCs在响应CCL5.5时表现出增加的运动性和传递性.
- 在感染后,小鼠在血液和脑血管中表现出快速的CCL5上调.
- CCL5促进了受感染的DC粘附于大脑微血管,增加了寄生虫负载.
- CCR5抗剂马拉维罗克减少了大脑中受感染的DC封存.
结论:
- T. gondii利用宿主CCL5/CCR5轴进行白细胞依赖的传播到中枢神经系统.
- 寄生虫效应器GRA15驱动CCL5诱导,促进大脑的殖民.
关键词:
(MeSH):宿主病原体的病原体.血脑屏障是什么意思中枢神经系统 原生动物感染 中枢神经系统 原生动物感染化学物质 (chemokines) 是一种化学物质.细胞内寄生虫 细胞内寄生虫白细胞化学反应 (白细胞化学反应)更多相关视频
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