白细胞介素21
细胞生物学
穿孔素
白细胞介素12
Janus激酶3
生物
CD49b
淋巴因子激活杀伤细胞
细胞凋亡
细胞
先天免疫系统
免疫系统
免疫学
T细胞
细胞毒性T细胞
体外
CD8型
遗传学
作者
Nicole C. Guilz,Yong‐Oon Ahn,Hijab Fatima,Luis Alberto Pedroza,Seungmae Seo,Rajesh K. Soni,Ning Wang,Dieter Egli,Emily M. Mace
出处
期刊:Journal of Immunology
[American Association of Immunologists]
日期:2024-05-29
卷期号:213 (1): 40-51
被引量:1
标识
DOI:10.4049/jimmunol.2300843
摘要
Abstract NK cells are innate immune effectors that kill virally infected or malignant cells. NK cell deficiency (NKD) occurs when NK cell development or function is impaired and variants in MCM4, GINS1, MCM10, and GINS4 result in NKD. Although NK cells are strongly impacted by mutational deficiencies in helicase proteins, the mechanisms underlying this specific susceptibility are poorly understood. In this study, we induced replication stress in activated NK cells or T cells by chemical and genetic methods. We found that the CD56bright subset of NK cells accumulates more DNA damage and replication stress during activation than do CD56dim NK cells or T cells. Aphidicolin treatment increases apoptosis of CD56bright NK cells through increased pan-caspase expression and decreases perforin expression in surviving cells. These findings show that sensitivity to replication stress affects NK cell survival and function and contributes to NKD.
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