Seki S, Hashimoto W, Ogasawara K, Satoh M, Watanabe H, Habu Y, Hiraide H, Takeda K
Division of Basic Traumatology, National Defence Medical College Research Institute, Tokorozawa, Japan.
Immunology. 1997 Dec;92(4):561-6. doi: 10.1046/j.1365-2567.1997.00383.x.
Depletion of both natural killer 1.1+ (NK1+) intermediate alpha beta T-cell receptor (int T) cells and NK cells by in vivo treatment with anti-NK1 antibody greatly increased hepatic metastases of intravenously injected EL4 cells as well as pulmonary metastases of 3LL cells in C57BL/6 mice. However, depletion of NK cells alone by anti-asialo GM1 (AGM1) antibody treatment did not increase the metastases in either organ. Interleukin-12 (IL-12) administration into mice induced strong cytotoxicities of NK cell-depleted liver and lung mononuclear cells (MNC) comparable to those without NK-cell depletion and inhibited metastases in either organ. In contrast, in both NK cell- and NK1+ int T-cell-depleted mice, IL-12 could not induce cytotoxic activity of liver and lung MNC and metastases in both organs increased with or without IL-12 treatment. These results confirmed the fact that NK+ int T cells are more potent antitumour effectors than NK cells against experimental haematogenous tumour metastases.
通过用抗NK1抗体进行体内治疗，使自然杀伤性1.1 +（NK1 +）中间αβT细胞受体（int T）细胞和NK细胞均耗竭，可大大增加C57BL / 6小鼠静脉注射EL4细胞的肝转移以及3LL细胞的肺转移。然而，单独用抗去唾液酸GM1（AGM1）抗体治疗使NK细胞耗竭，并不会增加任一器官的转移。向小鼠体内注射白细胞介素-12（IL-12）可诱导NK细胞耗竭的肝和肺单核细胞（MNC）产生强大的细胞毒性，其与未进行NK细胞耗竭的情况相当，并可抑制任一器官的转移。相反，在NK细胞和NK1 + int T细胞均耗竭的小鼠中，IL-12无法诱导肝和肺MNC的细胞毒性活性，并且无论是否进行IL-12治疗，两个器官的转移均会增加。这些结果证实了一个事实，即NK + int T细胞在对抗实验性血源性肿瘤转移方面比NK细胞具有更强的抗肿瘤效应。
