细胞毒性T细胞
CTL公司*
效应器
翻译(生物学)
胞浆
细胞生物学
生物
CD8型
线粒体
生物化学
信使核糖核酸
免疫学
免疫系统
体外
酶
基因
作者
Miriam Lisci,P. Barton,Lyra O. Randzavola,Y. Claire,Julia M. Marchingo,Doreen A. Cantrell,Vincent Paupe,Julien Prudent,Jane C. Stinchcombe,Gillian M. Griffiths
出处
期刊:Science
[American Association for the Advancement of Science (AAAS)]
日期:2021-10-15
卷期号:374 (6565)
被引量:75
标识
DOI:10.1126/science.abe9977
摘要
Mitochondria drive CTLs’ killer instinct Cytotoxic T lymphocytes (CTLs) can terminate both virally infected cells and cancer cells by secreting cytolytic proteins such as perforin and granzyme B. CTLs are particularly effective because they can sequentially kill multiple targets in a process called serial killing. Lisci et al . have identified mitochondria as important regulators of CTL killing. Mice lacking the deubiquitinase USP30 have CTLs acutely depleted of mitochondria, and these cells have reduced killing ability but normal motility, signaling, and secretion. Surprisingly, the mitochondria’s metabolic functions were not required for this process. Rather, mitochondrial translation proved indispensable for CTL cytolytic protein synthesis and sustained CTL killing. —STS
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