异常的17型对缺乏T-bet和eomesodermin的CD8+T细胞的病毒感染的反应
Andrew M Intlekofer1, Arnob Banerjee, Naofumi Takemoto
1Abramson Family Cancer Research Institute, University of Pennsylvania, Philadelphia, PA 19104, USA.
概括
转录因子T-bet和eomesodermin (Eomes) 对于CD8+ T细胞成为细胞毒杀手对抗细胞内病原体至关重要. 没有它们,CD8+ T细胞会促进有害的炎症,而不是有效的病毒防御.
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:
- CD8+ T 细胞对于控制细胞内病原体感染至关重要.
- 细胞毒性CD8+ T细胞消除受感染的细胞并分泌细胞因子.
- CD8+ T 细胞的分化途径是宿主防御的关键.
研究的目的:
- 研究转录因子T-bet和eomesodermin (Eomes) 在病毒感染期间 CD8+ T 细胞分化中的作用.
- 确定缺乏T-bet和Eomes对免疫反应和宿主病理学的后果.
主要方法:
- 在缺乏T-bet和Eomes的小鼠中分析CD8+T细胞分化.
- 使用淋巴细胞胆膜炎病毒 (LCMV) 的感染模型.
- 评估T细胞系承诺和宿主炎症反应.
主要成果:
- 缺乏T-bet和Eomes的CD8+T细胞无法发展成为细胞毒杀手.
- 这些细胞分化为类似T辅助体的,分泌互白素-17的细胞系.
- 在T细胞中缺乏T-bet和Eomes的小鼠会发展出一种严重的炎症综合征,其特征是中性粒细胞透.
结论:
- T-bet和Eomes对于引导CD8+T细胞向有效的细胞毒性效应因子功能对抗细胞内病原体至关重要.
- 这些因素的缺失导致异常的CD8+T细胞分化,促进有害的炎症和自身免疫性病理.
- 这些转录因子确保在病毒感染期间CD8+ T细胞的适当细胞毒性,而不是辅助性命运.
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