{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,15]],"date-time":"2026-05-15T15:10:06Z","timestamp":1778857806316,"version":"3.51.4"},"reference-count":0,"publisher":"Cell Physiol Biochem Press GmbH and Co KG","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Cell Physiol Biochem"],"abstract":"<jats:p>BACKGROUND\/AIMS: During an immune response, type I interferon (IFN-I) signaling induces a wide range of changes, including those which are required to overcome viral infection and those which suppress cytotoxic T cells to avoid immunopathology. During certain bacterial infections, IFN-I signaling exerts largely detrimental effects. Although the IFN-I family of proteins all share one common receptor, biologic responses to signaling vary depending on IFN-I subtype. Here, we asked if one IFN-I subtype dominates the pro-bacterial effect of IFN-I signaling and found that control of Listeria monocytogenes (L.m.) infection is more strongly suppressed by IFN-\u03b2 than IFN-\u03b1. METHODS: To study this, we measured bacterial titers in IFNAR-\/-, IFN-\u03b2\u2011\/\u2011, Stat2-\/-, Usp18fl\/fl and Usp18fl\/fl x CD11c-Cre mice models in addition to IFN-I blocking antibodies. Moreover, we measured interferon stimulated genes in bone marrow derived dendritic cells after treatment with IFN-\u03b14 and IFN-\u03b2. RESULTS: Specifically, we show that genetic deletion of IFN-\u03b2 or antibody-mediated IFN-\u03b2 neutralization was sufficient to reduce bacterial titers to levels similar to those observed in mice that completely lack IFN-I signaling (IFNAR-\/- mice). However, IFN-\u03b1 blockade failed to significantly reduce L.m. titers, suggesting that IFN-\u03b2 is the dominant IFN-I subtype responsible for the pro-bacterial effect of IFN-I. Mechanistically, when focusing on IFN-I signals to dendritic cells, we found that IFN-\u03b2 induces ISGs more robustly than IFN-\u03b1, including USP18, the protein we previously identified as driving the pro-bacterial effects of IFN-I. Further, we found that this induction was STAT1\/STAT2 heterodimer- or STAT2\/STAT2 homodimer-dependent, as STAT2-deficient mice were more resistant to L.m. infection. CONCLUSION: In conclusion, IFN-\u0392 is the principal member of the IFN-I family responsible for driving the pro-bacterial effect of IFN-I.<\/jats:p>","DOI":"10.33594\/000000370","type":"journal-article","created":{"date-parts":[[2021,5,13]],"date-time":"2021-05-13T15:59:08Z","timestamp":1620921548000},"page":"256-264","source":"Crossref","is-referenced-by-count":9,"title":["IFN-\u03b2, but not IFN-\u03b1, is Responsible for the Pro-Bacterial Effect of Type I Interferon"],"prefix":"10.33594","volume":"55","member":"19235","published-online":{"date-parts":[[2021,5,14]]},"container-title":["Cellular Physiology and Biochemistry"],"original-title":[],"deposited":{"date-parts":[[2021,5,13]],"date-time":"2021-05-13T15:59:08Z","timestamp":1620921548000},"score":1,"resource":{"primary":{"URL":"https:\/\/www.cellphysiolbiochem.com\/Articles\/000370\/"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2021,5,14]]},"references-count":0,"journal-issue":{"issue":"3","published-online":{"date-parts":[[2021,5,14]]}},"URL":"https:\/\/doi.org\/10.33594\/000000370","relation":{},"ISSN":["1015-8987","1421-9778"],"issn-type":[{"value":"1015-8987","type":"print"},{"value":"1421-9778","type":"electronic"}],"subject":[],"published":{"date-parts":[[2021,5,14]]}}}