Interferon lambda in respiratory viral infection: immunomodulatory functions and antiviral effects in epithelium

Front Immunol. 2024 Mar 1:15:1338096. doi: 10.3389/fimmu.2024.1338096. eCollection 2024.

Abstract

Type III interferon (IFN-λ), a new member of the IFN family, was initially considered to possess antiviral functions similar to those of type I interferon, both of which are induced via the JAK/STAT pathway. Nevertheless, recent findings demonstrated that IFN-λ exerts a nonredundant antiviral function at the mucosal surface, preferentially produced in epithelial cells in contrast to type I interferon, and its function cannot be replaced by type I interferon. This review summarizes recent studies showing that IFN-λ inhibits the spread of viruses from the cell surface to the body. Further studies have found that the role of IFN-λ is not only limited to the abovementioned functions, but it can also can exert direct and/or indirect effects on immune cells in virus-induced inflammation. This review focuses on the antiviral activity of IFN-λ in the mucosal epithelial cells and its action on immune cells and summarizes the pathways by which IFN-λ exerts its action and differentiates it from other interferons in terms of mechanism. Finally, we conclude that IFN-λ is a potent epidermal antiviral factor that enhances the respiratory mucosal immune response and has excellent therapeutic potential in combating respiratory viral infections.

Keywords: immunity; inflammation; interferon lambda; respiratory tract; type III interferon; viral infection.

Publication types

  • Review
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antiviral Agents / pharmacology
  • Antiviral Agents / therapeutic use
  • Epithelium / metabolism
  • Humans
  • Interferon Lambda
  • Interferon Type I* / metabolism
  • Janus Kinases / metabolism
  • STAT Transcription Factors / metabolism
  • Signal Transduction
  • Virus Diseases*

Substances

  • Interferon Lambda
  • Janus Kinases
  • STAT Transcription Factors
  • Interferon Type I
  • Antiviral Agents

Grants and funding

The author(s) declare that financial support was received for the research, authorship, and/or publication of this article. This work was supported by the CAMS Innovation Fund for Medical Sciences (CIFMS, 2021-I2M-1-048) and the National Natural Science Foundation of China (82204739).