期刊
NATURE IMMUNOLOGY
卷 16, 期 12, 页码 1215-1227出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ni.3279
关键词
-
类别
资金
- US National Institutes of Health (National Institute of Allergy and Infectious Diseases Asthma and Allergic Diseases Cooperative Research Center) [U19-AI070489, U54-AI05160, RO1-AI111605, R15-AI099134]
- Martin Schaeffer Fund
Enhancing the response to interferon could offer an immunological advantage to the host. In support of this concept, we used a modified form of the transcription factor STAT1 to achieve hyper-responsiveness to interferon without toxicity and markedly improve antiviral function in transgenic mice and transduced human cells. We found that the improvement depended on expression of a PARP9-DTX3L complex with distinct domains for interaction with STAT1 and for activity as an E3 ubiquitin ligase that acted on host histone H2BJ to promote interferon-stimulated gene expression and on viral 3C proteases to degrade these proteases via the immunoproteasome. Thus, PARP9-DTX3L acted on host and pathogen to achieve a double layer of immunity within a safe reserve in the interferon signaling pathway.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据