The Key Roles of Interferon Lambda in Human Molecular Defense against Respiratory Viral Infections

Interferons (IFN) are crucial for the innate immune response. Slightly more than two decades ago, a new type of IFN was discovered: the lambda IFN (type III IFN). Like other IFN, the type III IFN display antiviral activity against a wide variety of infections, they induce expression of antiviral, in...

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Published in:Pathogens (Basel) Vol. 9; no. 12; p. 989
Main Authors: Lozhkov, Alexey A., Klotchenko, Sergey A., Ramsay, Edward S., Moshkoff, Herman D., Moshkoff, Dmitry A., Vasin, Andrey V., Salvato, Maria S.
Format: Journal Article
Language:English
Published: Switzerland MDPI AG 26.11.2020
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ISSN:2076-0817, 2076-0817
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Summary:Interferons (IFN) are crucial for the innate immune response. Slightly more than two decades ago, a new type of IFN was discovered: the lambda IFN (type III IFN). Like other IFN, the type III IFN display antiviral activity against a wide variety of infections, they induce expression of antiviral, interferon-stimulated genes (MX1, OAS, IFITM1), and they have immuno-modulatory activities that shape adaptive immune responses. Unlike other IFN, the type III IFN signal through distinct receptors is limited to a few cell types, primarily mucosal epithelial cells. As a consequence of their greater and more durable production in nasal and respiratory tissues, they can determine the outcome of respiratory infections. This review is focused on the role of IFN-λ in the pathogenesis of respiratory viral infections, with influenza as a prime example. The influenza virus is a major public health problem, causing up to half a million lethal infections annually. Moreover, the virus has been the cause of four pandemics over the last century. Although IFN-λ are increasingly being tested in antiviral therapy, they can have a negative influence on epithelial tissue recovery and increase the risk of secondary bacterial infections. Therefore, IFN-λ expression deserves increased scrutiny as a key factor in the host immune response to infection.
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ISSN:2076-0817
2076-0817
DOI:10.3390/pathogens9120989