Reichlin A, Yokoyama W M
Department of Pediatrics, Washington University School of Medicine, St Louis, Missouri 63110, USA.
Immunol Cell Biol. 1998 Apr;76(2):143-52. doi: 10.1046/j.1440-1711.1998.00726.x.
NKR-P1 molecules are involved in natural killing of certain tumour targets. Indeed, the NK1.1 (NKR-P1C) molecule is the most specific serological marker on murine NK cells in C57BL/6 mice. Previous studies of NKR-P1 have indicated that anti-NKR-P1 mAb induced NK cells to kill otherwise insensitive targets, NK cell phosphoinositol turnover and Ca++ flux but it was not previously known if all NK cells were activated. In this study we report that immobilized anti-NK1.1 also specifically induced proliferation as measured by thymidine incorporation. The response required low doses of IL-2 for a synergistic effect. Cells stimulated with anti-NK1.1 + IL-2 displayed characteristic cytolytic activity against a NK-sensitive tumour target, YAC-1. However, anti-NK1.1-stimulated cells displayed delayed proliferation kinetics, heterogeneity of the expression of the very early antigen marker, CD69, and altered expression of the Ly-49 family members when compared to NK cells activated by high concentrations of IL-2. Taken together, these data demonstrate that immobilized anti-NK1.1 triggers only a subpopulation of NK cells.
NKR - P1分子参与对某些肿瘤靶标的自然杀伤作用。实际上,NK1.1(NKR - P1C)分子是C57BL/6小鼠中鼠自然杀伤细胞上最具特异性的血清学标志物。先前对NKR - P1的研究表明,抗NKR - P1单克隆抗体可诱导自然杀伤细胞杀伤原本不敏感的靶标,引起自然杀伤细胞磷酸肌醇周转和钙离子通量,但此前尚不清楚是否所有自然杀伤细胞均被激活。在本研究中,我们报告称,通过胸苷掺入法测定,固定化抗NK1.1也能特异性诱导细胞增殖。该反应需要低剂量白细胞介素 - 2产生协同效应。用抗NK1.1 +白细胞介素 - 2刺激的细胞对自然杀伤细胞敏感的肿瘤靶标YAC - 1表现出特征性细胞溶解活性。然而,与高浓度白细胞介素 - 2激活的自然杀伤细胞相比,抗NK1.1刺激的细胞增殖动力学延迟,极早期抗原标志物CD69表达存在异质性,且Ly - 49家族成员的表达发生改变。综上所述,这些数据表明固定化抗NK1.1仅触发自然杀伤细胞的一个亚群。