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在弗朗西塞拉菌感染后,巨细胞的脱化酶的活性发生变化
Vera Vozandychova1, Pavel Rehulka1, Kamil Hercik1,2
1Department of Molecular Pathology and Biology, Faculty of Military Health Sciences, University of Defence, Hradec Kralove, Czechia.
Frontiers in immunology
|October 16, 2023
概括
弗朗西塞拉 (Francisella tularensis) 感染通过增加duibiquitinating酶 (DUB) 活性来改变宿主泛化. 特定的DUBs如USP10,UCH-L5和USP25在外体中发现,影响宿主免疫反应.
科学领域:
- 免疫学 免疫学 免疫学
- 分子生物学分子生物学
- 细胞微生物学 细胞微生物学
背景情况:
- 乌比基因化和二维基因化是细胞信号传递和蛋白质降解中的关键调节过程.
- 像Francisella tularensis这样的细胞内病原体经常操纵宿主分子通路,以逃避免疫反应.
- 众所周知,弗朗西塞拉 (Francisella tularensis) 感染会影响宿主信号通路,但其对无处不在的作用尚未完全理解.
研究的目的:
- 研究弗朗西塞拉 (Francisella tularensis) 感染对巨细胞宿主泛化和双化机制的影响.
- 为了识别受Francisella tularensis感染影响的特定二氧化酶 (DUBs).
- 为了确定感染期间受影响的DUBs的局部.
主要方法:
- 人类巨细胞感染弗朗西塞拉tularensis.
- 测定总二维基素化酶 (DUB) 活性.
- 对特定的DUB进行酶活性测定 (USP10,UCH-L5,USP25).
- 外体隔离和对DUB丰富的分析.
主要成果:
- 弗朗西塞拉 (Francisella tularensis) 感染导致人体巨细胞中DUB总活性增加.
- 减少USP10和UCH-L5的酶活性,而增加USP25的活性.
- 发现USP10,UCH-L5和USP25富含来自受感染细胞的外体.
结论:
- 弗朗西塞拉 (Francisella tularensis) 活跃地干扰宿主的无处不在系统.
- 病原体调节特定DUBs的活性,潜在地逃避降解和操纵宿主反应.
- 这些DUB在外体中的丰富表明细胞间通信或免疫逃避的机制.
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