Enhanced tumor development in mice lacking a functional type I interferon receptor
Enhanced tumor development in mice lacking a functional type I interferon receptor
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DOI：
10.1089/10799900252952244
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发表时间：
2002-04-01
影响因子：
2.3
通讯作者：
Seif, I
中科院分区：
文献类型：
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作者：
Picaud, S;Bardot, B;Seif, I
本研究的目的是研究内源性的贡献，即不添加任何干扰素（IFN）诱导剂I型IFN的产生在防御肿瘤发展中的作用。为此，通过10代回交，将ifn - α受体（IFNAR）敲除（KO）诱导的突变引入C3H遗传背景，导致ifn - α / β活性完全缺失，然后进行至少4代的兄弟姐妹交配。小鼠分别接种同种C3H黑色素瘤K1735细胞、同种异体3LL癌细胞或同种异体B16F10黑色素瘤细胞。在这三种肿瘤细胞系中，IFNAR KO动物的肿瘤发展和随后的死亡率都有所提高。这表明内源性ifn - α / β的产生是对肿瘤发展的自然免疫的中介。
The aim of this study was to investigate the contribution of endogenous-that is, without the addition of any interferon (IFN) inducer-type I IFN production in the defense against tumor development. To this purpose, the IFN-alpha receptor (IFNAR) knockout (KO)-induced mutation, resulting in the complete absence of IFN-alpha/beta activity, was introduced into a C3H genetic background by 10 backcross generations, followed by brother-sister matings for at least four generations. The resulting mice were inoculated either with syngeneic C3H melanoma K1735 cells, with allogeneic 3LL carcinoma cells, or with allogeneic B16F10 melanoma cells. With all three tumor cell lines, tumor development and ensuing mortality were enhanced in the IFNAR KO animals. This indicates that endogenous IFN-alpha/beta production is a mediator of natural immunity to tumor development.