Enhanced tumor development in mice lacking a functional type I interferon receptor

被引：44

作者：

Picaud, S ^{[1
]}

Bardot, B ^{[1
]}

De Maeyer, E ^{[1
]}

Seif, I ^{[1
]}

机构：

[1] Inst Pasteur, Ctr Univ Orsay, F-91400 Orsay, France

来源：

JOURNAL OF INTERFERON AND CYTOKINE RESEARCH | 2002年 / 22卷 / 04期

关键词：

D O I：

10.1089/10799900252952244

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

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.

引用

页码：457 / 462

页数：6

共 16 条

[1] The neglected role of type I interferon in the T-cell response: Implications for its clinical use [J].