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

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    Author
    Lozhkov, Alexey A
    Klotchenko, Sergey A
    Ramsay, Edward S
    Moshkoff, Herman D
    Moshkoff, Dmitry A
    Vasin, Andrey V
    Salvato, Maria S
    Date
    2020-11-26
    Journal
    Pathogens (Basel, Switzerland)
    Publisher
    MDPI AG
    Type
    Article
    Other
    
    Metadata
    Show full item record
    See at
    https://doi.org/10.3390/pathogens9120989
    Abstract
    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.
    Keyword
    influenza
    innate immunity
    interferon stimulated genes
    interferons-α/β
    interferons-λ
    respiratory viruses
    Identifier to cite or link to this item
    http://hdl.handle.net/10713/14178
    ae974a485f413a2113503eed53cd6c53
    10.3390/pathogens9120989
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