Research ArticleINFECTIOUS DISEASES

The probacterial effect of type I interferon signaling requires its own negative regulator USP18

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Science Immunology  28 Sep 2018:
Vol. 3, Issue 27, eaau2125
DOI: 10.1126/sciimmunol.aau2125

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  • RE: The probacterial effect of type I interferon signaling requires its own negative regulator USP18
    • Dr Dianne Sika-Paotonu, Associate Dean (Pacific)/Senior Lecturer Pathology & Molecular Medicine, Wellington School of Medicine & Health Sciences, University of Otago, New Zealand

    To the Editor,

    I read with interest the article authored by Shaabani N. et al (1) and entitled: “The probacterial effect of type 1 interferon (IFN-I) signalling requires its own negative regulator USP18”.

    This work explored the role of the interferon-stimulated gene and negative regulator of IFN-I signalling Usp18, and showed that Usp18 was responsible for the damaging impact of IFN-I signalling that occurred during infection with Listeria monocytogenes and Staphylococcus aureus.

    The authors also investigated the mechanism for the IFN-I associated increased susceptibility to bacterial infection and demonstrated that USP18 promoted bacterial infection by inhibiting antibacterial tumour necrosis factor-a (TNF-a) signalling and reduced subsequent reactive oxygen species (ROS) production.

    To induce secondary bacterial infection following viral infection with acute lymphocytic choriomeningitis virus (LCMV), murine recipients were subsequently exposed to Listeria monocytogenes. In addition a TLR 3 agonist was used to induce IFN-I and further explore the role of USP18. This focus demonstrated across a series of experiments that the probacterial role of IFN-I during superinfection is USP-18 dependent.

    Another key point of interest was the proposal that therapeutic targeting of USP18 could allow diseases caused by M. tuberculosis, Francisella tularensis, S. typhimurium and S. aureus to be treated without affecting the IFN-I signalling needed to...

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    Competing Interests: None declared.

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