细胞死亡调节器c-FLIPR在流感病毒感染期间损害了自然杀手细胞的反应
André Carmo-Fernandes1, Neda Tafrishi2, Clara Bessen1
1Department of Molecular Immunology, Medical Faculty, Ruhr University Bochum, Universitaetsstrasse 150, 44801, Bochum, Germany.
概括
在血液细胞中,细胞FLICE抑制蛋白R (c-FLIPR) 的构成表达增强了流感A病毒 (IAV) 的复制. 这项研究揭示了c-FLIPR在IAV感染期间损害了自然杀手 (NK) 细胞功能.
科学领域:
- 免疫学 免疫学 免疫学
- 病毒学 病毒学
- 细胞生物学 细胞生物学
背景情况:
- 亡对于感染期间的恒温至关重要.
- 细胞FLICE抑制蛋白 (c-FLIP) 调节细胞亡; c-FLIPR的功能尚不清楚.
- 甲型流感病毒 (IAV) 感染会影响宿主免疫反应.
研究的目的:
- 调查c-FLIPR在IAV感染中的作用.
- 分析c-FLIPR对IAV感染期间自然杀手 (NK) 细胞活性的影响.
主要方法:
- 使用了在血液细胞中表达小鼠c-FLIPR的转基因小鼠.
- 具有IAV的挑战性小鼠和评估的病毒载量和免疫细胞群.
- 在体外和体内评估NK细胞脱粒化,TNFα和IFNg表达.
主要成果:
- vavFLIPR小鼠在IAV挑战后表现出更高的病毒载量.
- 艾滋病毒感染导致VavFLIPR小鼠NK细胞数量增加.
- 在IAV感染后,c-FLIPR转基因NK细胞显示降低了脱粒化和降低了TNFα/IFNg表达.
- IAV有效地感染NK细胞,但病毒颗粒不会感染其他细胞.
结论:
- 在造血细胞中构成性c-FLIPR表达会加剧IAV感染.
- 在IAV感染期间,c-FLIPR会损害NK细胞的抗病毒活性.
- NK细胞是IAV的目标,它们的功能受到病毒的影响.
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