Minakuchi J, Yata J
Department of Pediatrics, Faculty of Medicine, Tokyo Medical and Dental University.
Tohoku J Exp Med. 1988 Jun;155(2):107-15. doi: 10.1620/tjem.155.107.
When peripheral blood lymphocytes from healthy adults are cultured with autologous (auto) or allogeneic (allo) Epstein-Barr virus-transformed cells (LCL), non-specific killer activity against NK-sensitive K562 and NK-resistant Raji, as well as specific killer activity against LCL is enhanced or generated. We analyzed the cell subsets possessing such cytotoxicity using monoclonal antibodies (MoAb). OKT3, a MoAb to T cell receptor-associated molecule, added in the effector phase suppressed the killer activity against LCL but not against Raji or K562. In contrast, OKT3 added in the induction phase abolished the generation of cytotoxicity against all targets. The addition of OKT8 in either the effector or induction phase inhibited anti-LCL killing induced by stimulation with alloLCL. This suggests that CD8 is required for recognition of alloLCL. The treatment of effector cells with MoAb and complement(C) revealed that killers against LCL were OKT8+ Leu11-, and those against K562 were OKT8- Leu11+. When auto-LCL were used as stimulator, removal of OKT4+ cells in the induction phase diminished the cytotoxicity against all targets, indicating that CD4+ T cells recognize autoLCL. Elimination of CD8+ cells from responder did not decrease the generation of killer activity. Further experiments suggested that this was caused by the coexistence of CD4+ killer cells or by the increase of residual CD8+ effector cells.
当将健康成年人的外周血淋巴细胞与自体(自身)或异体(同种异体)爱泼斯坦 - 巴尔病毒转化细胞(LCL)共同培养时,针对NK敏感的K562和NK抗性的Raji的非特异性杀伤活性以及针对LCL的特异性杀伤活性会增强或产生。我们使用单克隆抗体(MoAb)分析了具有这种细胞毒性的细胞亚群。效应阶段添加的OKT3,一种针对T细胞受体相关分子的MoAb,抑制了针对LCL的杀伤活性,但不抑制针对Raji或K562的杀伤活性。相反,诱导阶段添加的OKT3消除了对所有靶标的细胞毒性的产生。效应阶段或诱导阶段添加OKT8均抑制了同种异体LCL刺激诱导的抗LCL杀伤作用。这表明CD8是识别同种异体LCL所必需的。用MoAb和补体(C)处理效应细胞表明,针对LCL的杀伤细胞是OKT8 + Leu11 -,而针对K562的杀伤细胞是OKT8 - Leu11 +。当使用自身LCL作为刺激物时,诱导阶段去除OKT4 +细胞会降低对所有靶标的细胞毒性,表明CD4 + T细胞识别自身LCL。从反应细胞中消除CD8 +细胞不会降低杀伤活性的产生。进一步的实验表明,这是由CD4 +杀伤细胞的共存或残留CD8 +效应细胞的增加引起的。