While an appropriately regulated production of interferons (IFNs) performs a fundamental role in the defense against coronaviruses such as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), dysregulated overproduction of inflammatory mediators can play an important role in the development of SARS-CoV-2 infection-related complications, such as acute respiratory distress syndrome. As the principal constituents of innate immunity, both type I and III IFNs share antiviral features. However, important properties, including preferential expression at mucosal barriers (such as respiratory tract), local influences, lower receptor distribution, smaller target cell types, noninflammatory effects, and immunomodulatory impacts, were attributed only to type III IFNs. Accordingly, type III IFNs can establish an optimal effective antiviral response, without triggering exaggerated systemic inflammation that is generally attributed to the type I IFNs. However, some harmful effects were attributed to the III IFNs and there are also major differences between human and mouse concerning the immunomodulatory effects of III IFNs. Here, we describe the differential properties of type I and type III IFNs and present a model of IFN response during SARS-COV-2 infection, while highlighting the superior potential of type III IFNs in COVID-19.

中文翻译：

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III 型干扰素对 COVID-19 患者的保护潜力：来自 I 型和 III 型干扰素不同特性的经验教训

虽然干扰素 (IFN) 的适当调节生产在防御冠状病毒如严重急性呼吸系统综合症冠状病毒 2 (SARS-CoV-2) 方面发挥着重要作用，但炎症介质的失调过度生产可能在 SARS 的发展中发挥重要作用-CoV-2 感染相关并发症，例如急性呼吸窘迫综合征。作为先天免疫的主要成分，I 型和 III 型干扰素都具有抗病毒特性。然而，重要的特性，包括在粘膜屏障（如呼吸道）的优先表达、局部影响、较低的受体分布、较小的靶细胞类型、非炎症效应和免疫调节影响，仅归因于 III 型干扰素。因此，III 型干扰素可以建立最佳的有效抗病毒反应，不会引发通常归因于 I 型干扰素的过度全身炎症。然而，一些有害影响归因于 III 型干扰素，并且人类和小鼠之间在 III 型干扰素的免疫调节作用方面也存在重大差异。在这里，我们描述了 I 型和 III 型 IFN 的不同特性，并提出了 SARS-COV-2 感染期间的 IFN 反应模型，同时强调了 III 型 IFN 在 COVID-19 中的优越潜力。