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.

I 型干扰素 (IFN-I) 对于抗病毒免疫至关重要的概念源自对动物模型和细胞系的研究。事实上，所有致病病毒都已进化出针对 IFN-I 限制的对策，病毒 IFN-I 拮抗剂的遗传缺失会导致病毒减毒。但 IFN-I 对于人类抗病毒防御到底有多重要呢？最近发现的 IFN-I 信号传导的遗传缺陷阐明了 IFN 生物学的这一问题和其他问题，包括粘膜限制性 III 型 IFN (IFN-III) 的作用，使我们了解 IFN 系统在协同作用中的地位。抗病毒反应。在这里，我们回顾了 IFN-I 信号通路的单基因损伤，并总结了出现的组织原则。