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Targeted disruption of the mouse STAT1 results in compromised innate immunity to viral disease

被引：1309
作者：
Durbin, JE
Hackenmiller, R
Simon, MC
Levy, DE
机构：
[1] NYU,SCH MED,DEPT PATHOL,NEW YORK,NY 10016
[2] NYU,SCH MED,KAPLAN CANC CTR,NEW YORK,NY 10016
[3] UNIV CHICAGO,DEPT MED,CHICAGO,IL 60637
[4] UNIV CHICAGO,HOWARD HUGHES MED INST,CHICAGO,IL 60637
来源：
CELL | 1996年 / 84卷 / 03期
基金：
美国国家卫生研究院;
关键词：
D O I：
10.1016/S0092-8674(00)81289-1
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 STAT1 transcription factor is activated in response to many cytokines and growth factors. To study the requirement for STAT1 in vivo, we disrupted the Stat1 gene in embryonic stem (ES) cells and in mice. Stat1(-/-) ES cells were unresponsive to interferon (IFN), but retained responsiveness to leukemia inhibitory factor (LIF) and remained LIF dependent for undifferentiated growth. Stat1(-/-) animals were born at normal frequencies and displayed no gross developmental defects. However, these animals failed to thrive and were extremely susceptible to viral disease. Cells and tissues from Stat1(-/-) mice were unresponsive to IFN, but remained responsive to all other cytokines tested. Thus, STAT1 appears to be specific for IFN pathways that are essential for viability in the face of otherwise innocuous pathogens.
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页码：443 / 450
页数：8
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