NK cells rapidly remove B16F10 tumor cells in a perforin and interferon-gamma independent manner in vivo

被引:36
作者
Grundy, Martin A.
Zhang, Tong
Sentman, Charles L.
机构
[1] Department of Microbiology and Immunology, Dartmouth Medical School, 6W Borwell Building, Lebanon, NH 03756, One Medical Center Drive
关键词
lung; tumor metastasis; gene-deficient mice; confocal microscopy; tumor immunology; innate immunity;
D O I
10.1007/s00262-006-0264-1
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Natural killer (NK) cells have been shown critical in reducing tumor lung metastasis in various murine cancer models. Effector molecules such as perforin and IFN-gamma may play important roles in inhibition of metastasis. However, most of these conclusions were based on experiments that involved quantitation of metastatic colonies several weeks after tumor challenge. The roles of NK cells and their effector molecules (perforin and IFN-gamma) in the initial immune responses against tumor metastasis in lungs are still unknown. By using the B16F10 melanoma tumor model combined with confocal microscopy, we observed an increase in numbers of B16F10 cells in NK-depleted mice at 60 min post tumor inoculation, but this effect was independent of perforin or IFN-gamma. In addition, NK cell numbers in lungs after tumor injection rapidly increased suggesting a redistribution of NK cells in the lungs. However, NK cells were not found in contact with tumor cells until day 6 or later. Our data indicate that during early responses against B16F10 cells, NK cells use another mechanism(s) besides perforin and IFN-gamma to prevent tumor metastasis.
引用
收藏
页码:1153 / 1161
页数:9
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