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    Suppressor of cytokine signaling (SOCS)5 ameliorates influenza infection via inhibition of EGFR signaling

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    Author
    Kedzierski, L; Tate, MD; Hsu, AC; Kolesnik, TB; Linossi, EM; Dagley, L; Dong, Z; Freeman, S; Infusini, G; Starkey, MR; ...
    Date
    2017-02-14
    Source Title
    eLife
    Publisher
    ELIFE SCIENCES PUBLICATIONS LTD
    University of Melbourne Author/s
    Babon, Jeffrey; Linossi, Edmond; BIRD, NICOLA; Huntington, Nicholas; Belz, Gabrielle; Kedzierska, Katherine; Nicholson, Sandra; Dagley, Laura; Kedzierski, Lukasz; Infusini, Giuseppe; ...
    Affiliation
    Medical Biology (W.E.H.I.)
    Microbiology and Immunology
    Veterinary and Agricultural Sciences
    Metadata
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    Document Type
    Journal Article
    Citations
    Kedzierski, L., Tate, M. D., Hsu, A. C., Kolesnik, T. B., Linossi, E. M., Dagley, L., Dong, Z., Freeman, S., Infusini, G., Starkey, M. R., Bird, N. L., Chatfield, S. M., Babon, J. J., Huntington, N., Belz, G., webb, A., Wark, P. A. B., Nicola, N. A., Xu, J. ,... Nicholson, S. E. (2017). Suppressor of cytokine signaling (SOCS)5 ameliorates influenza infection via inhibition of EGFR signaling. ELIFE, 6, https://doi.org/10.7554/eLife.20444.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/258026
    DOI
    10.7554/eLife.20444
    Abstract
    Influenza virus infections have a significant impact on global human health. Individuals with suppressed immunity, or suffering from chronic inflammatory conditions such as COPD, are particularly susceptible to influenza. Here we show that suppressor of cytokine signaling (SOCS) five has a pivotal role in restricting influenza A virus in the airway epithelium, through the regulation of epidermal growth factor receptor (EGFR). Socs5-deficient mice exhibit heightened disease severity, with increased viral titres and weight loss. Socs5 levels were differentially regulated in response to distinct influenza viruses (H1N1, H3N2, H5N1 and H11N9) and were reduced in primary epithelial cells from COPD patients, again correlating with increased susceptibility to influenza. Importantly, restoration of SOCS5 levels restricted influenza virus infection, suggesting that manipulating SOCS5 expression and/or SOCS5 targets might be a novel therapeutic approach to influenza.

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