期刊
TRENDS IN GENETICS
卷 37, 期 1, 页码 46-58出版社
CELL PRESS
DOI: 10.1016/j.tig.2020.08.017
关键词
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资金
- Wellcome Trust [211153/Z/18/Z, 207556/Z/17/Z, 101788/Z/13/Z]
- Sir Jules Thorn Trust [12/JTA]
- British Medical Association
- Wellcome Trust [101788/Z/13/Z, 207556/Z/17/Z, 211153/Z/18/Z] Funding Source: Wellcome Trust
IFN-I is essential in antiviral immunity, with most pathogenic viruses evolving countermeasures against it. Recent discoveries of genetic defects in IFN-I signaling shed light on the importance of IFN-III in humans, enhancing our understanding of the role of the IFN system in the antiviral response.
The concept that type I interferons (IFN-I) are essential to antiviral immunity derives from studies on animal models and cell lines. Virtually all pathogenic viruses have evolved countermeasures to IFN-I restriction, and genetic loss of viral IFN-I antagonists leads to virus attenuation. But just how important is IFN-I to antiviral defence in humans? The recent discovery of genetic defects of IFN-I signalling illuminates this and other questions of IFN biology, including the role of the mucosa-restricted type III IFNs (IFN-III), informing our understanding of the place of the IFN system within the concerted antiviral response. Here we review monogenic lesions of IFN-I signalling pathways and summarise the organising principles which emerge.
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