Heiskala M K, Carpén O, Saksela E, Timonen T
J Immunol. 1987 Sep 1;139(5):1414-8.
Natural killer cell activity is inhibited by primary cultures of monolayer cells. In this study, we analyzed the mechanism of the inhibition. Inhibited NK cells showed unaltered binding capacity to NK sensitive K562 cells. The orientation of the effector cells' actin-containing microfilaments, an event known to occur during the programming for the lysis stage in lytic conjugates, was unaffected by the inhibition. In single cell cytotoxicity experiments, the number of killer cells among conjugate-forming cells was reduced. The capacity of the inactivated NK cells to secrete cytotoxic factors upon stimulation with Con A was also impaired. Both NK-resistant inactivating target cells and NK-sensitive K562 cells were sensitive to the toxic factors secreted by NK cells. Thus, the results indicate that the target cell-mediated inactivation of NK cell is based on a block in the lethal hit stage, possibly due to reduced release of toxic factor(s) from the effector cells. The capacity of inactivated effector cells to mediate antibody-dependent cellular cytotoxicity was unimpaired, suggesting that the contact-mediated inhibition of cytotoxicity selectively affects NK cells.
自然杀伤细胞活性受到单层细胞原代培养物的抑制。在本研究中，我们分析了这种抑制的机制。受抑制的自然杀伤细胞对自然杀伤敏感的K562细胞的结合能力未发生改变。效应细胞含肌动蛋白的微丝的取向，这是已知在溶细胞共轭物裂解阶段编程过程中发生的事件，不受该抑制的影响。在单细胞细胞毒性实验中，形成共轭物的细胞中杀伤细胞的数量减少。用刀豆球蛋白A刺激时，失活的自然杀伤细胞分泌细胞毒性因子的能力也受损。自然杀伤抗性失活靶细胞和自然杀伤敏感的K562细胞对自然杀伤细胞分泌的毒性因子均敏感。因此，结果表明靶细胞介导的自然杀伤细胞失活是基于致死性打击阶段的阻断，可能是由于效应细胞毒性因子释放减少所致。失活的效应细胞介导抗体依赖性细胞毒性的能力未受损，这表明接触介导的细胞毒性抑制选择性地影响自然杀伤细胞。
