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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Turning the tables on interferon

An early step in the host response to viral infection involves a burst of synthesis of type I interferons that allow cells to quickly fight back against the offending viruses. Shaabani et al. investigated how the same interferon-stimulated genes (ISGs) that usually help against viruses surprisingly dampen the host’s ability to resist many bacterial infections. Deletion of a single ISG known as Usp18 in mouse dendritic cells was sufficient to enhance host control of infections with two strains of Gram-positive bacteria. Normal induction of USP18 after infection impaired antibacterial responses mediated by tumor necrosis factor. These findings spotlight USP18 as a new potential target for therapeutics aimed at improving control of serious bacterial infections.