Cancer Immunology Research Unit, The Canberra Hospital, Australian Capital Territory, Australia.
J Immunol Methods. 2011 Jul 29;370(1-2):86-92. doi: 10.1016/j.jim.2011.06.002. Epub 2011 Jun 15.
The interaction of natural killer cells with susceptible target cells triggers NK cell activation, eliciting not only NK cell cytotoxicity and cytokine secretion, but also NK cell death. This study shows that following target cell interaction there is a substantial loss of NK cells, the extent of which correlates with measures of NK cell cytotoxicity assessed by the target cell release of (51)Cr and by the externalisation of the lysosomal marker LAMP-1 (CD107a) which is assessed on the remaining NK cells. This is the case for the killing of K562 (natural killing) and the CD20 mAb (Rituximab)-mediated killing of RAJI cells and autologous B cells (antibody-dependent cell cytotoxicity). This target-induced NK loss (TINKL) provides a sensitive and specific measure of NK cell responses appropriate to a clinical laboratory setting.
自然杀伤细胞与易感性靶细胞的相互作用触发 NK 细胞的激活，不仅引发 NK 细胞的细胞毒性和细胞因子分泌，还引发 NK 细胞的死亡。本研究表明，在靶细胞相互作用后，NK 细胞大量丢失，其丢失程度与通过靶细胞释放 (51)Cr 和通过溶酶体标记物 LAMP-1（CD107a）的外化来评估的 NK 细胞细胞毒性的测量值相关，后者是在剩余的 NK 细胞上进行评估的。这适用于 K562（自然杀伤）的杀伤以及 CD20 mAb（利妥昔单抗）介导的 RAJI 细胞和自体 B 细胞（抗体依赖性细胞毒性）的杀伤。这种靶诱导的 NK 细胞丢失（TINKL）提供了一种敏感和特异的 NK 细胞反应测量方法，适用于临床实验室环境。
