穿孔素
细胞毒性T细胞
淋巴因子激活杀伤细胞
颗粒酶
K562细胞
生物
白细胞介素21
Janus激酶3
细胞生物学
颗粒酶A
白细胞介素12
自然杀伤细胞
细胞外
NK-92
CD16
分子生物学
细胞
免疫学
免疫系统
CD8型
CD3型
生物化学
体外
作者
A.M. Shenov,Richard A. Sidner,Zacharie Brahmi
标识
DOI:10.1006/cimm.1993.1070
摘要
Our laboratory has previously demonstrated that natural killer (NK) cell-mediated cytotoxicity is protein kinase C (KC)-dependent and that PKC is translocated from the cytoplasm to the plasma membrane during NK cell activation. Furthermore, exposuring NK cells to a sensitive target cell for 4-6 hr at 37°C rendered NK cells functionally inactive and these inactivated effector cells (i) do not turn over Pl in response to K562 stimulation and (ii) lose mRNA for perforin and granzyme A and B less than 30 min after contact with K562. In this study, we first confirmed earlier findings that the interaction of sensitive target cells with human NK cells triggers an influx of extracellular calcium into NK cells. In addition, using flow cytometry we demonstrated that there was a delayed maximum uptake of extracellular calcium into functionally inactive NK cells when these cells were reexposed to fresh K562. Finally, we demonstrated that exposuring NK cells to K562 for hr leads to a loss of NK cytotoxic activity and to the maximal expression of CD69.
科研通智能强力驱动
Strongly Powered by AbleSci AI