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. 2020 Apr 14;217(5):e20200653. doi: 10.1084/jem.20200653

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© 2020 Prokunina-Olsson et al.

This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms/). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 International license, as described at https://creativecommons.org/licenses/by-nc-sa/4.0/).

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Figure 1. — Potential benefits of using type III IFNs for prevention and treatment of COVID-19 Type I IFNs (IFN-α/β) signal through a heterodimeric receptor complex, IFNAR, which is comprised of IFNAR1 and IFNAR2 subunits. IFNAR activation induces expression of ISGs and triggers pro-inflammatory responses via the recruitment and activation of immune cells. This promotes an antiviral state in the host, but as IFNAR is expressed on all cells, the administration of type I IFN can have serious systemic side effects. In contrast, type III IFNs (IFN-λ1-4) signal through a distinct receptor complex, IFNLR, which consists of IL10R2 and IFNLR1 subunits. IFNLR1 expression is restricted to epithelial cells and a subset of immune cells, including neutrophils. Therefore, type III IFN administration as a prophylactic treatment or at an early stage of COVID-19 would result in ISG expression and antiviral response localized to epithelial cells, reducing side effects and inflammation associated with the systemic action of type I IFNs.