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Antimetastatic effect of NK1+ T cells on experimental haematogenous tumour metastases in the liver and lungs of mice.

机译:NK1 + T细胞对小鼠肝和肺中实验性血源性肿瘤转移的抗转移作用。

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摘要

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.
机译:通过抗NK1抗体的体内处理耗尽自然杀手1.1+(NK1 +)中间αβT细胞受体(int T)细胞和NK细胞,大大增加了静脉注射EL4细胞的肝转移以及3LL的肺转移C57BL / 6小鼠体内的细胞。但是,仅通过抗亚洲GM1(AGM1)抗体处理而耗尽NK细胞并不会增加这两个器官中的转移。将白细胞介素12(IL-12)给予小鼠后,与没有NK细胞耗竭的小鼠相比,NK细胞耗竭的肝和肺单核细胞(MNC)产生了强烈的细胞毒性,并且在任一器官中均抑制了转移。相比之下,在NK细胞和NK1 +完整T细胞缺失的小鼠中,IL-12均不能诱导肝和肺MNC的细胞毒性活性,无论是否接受IL-12治疗,两个器官的转移均会增加。这些结果证实了NK + int T细胞比NK细胞对实验性血源性肿瘤转移更有效的抗肿瘤效应。

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