ArticlePLoS pathogens2012
Opposing roles for interferon regulatory factor-3 (IRF-3) and type I interferon signaling during plague.
Article in PLoS pathogens, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed.
- The dual role of type I interferons in bacterial infections: from immune defense to pathogenesis.mBio · 2025Review
- Pathogenicity and virulence ofVirulence · 2024Review
- Review
- Nod-like Receptors: Critical Intracellular Sensors for Host Protection and Cell Death in Microbial and Parasitic Infections.International journal of molecular sciences · 2021Review
- Impact of Type I Interferons on Susceptibility to Bacterial Pathogens.Trends in microbiology · 2021Review
- Enterobacteria and host resistance to infection.Mammalian genome : official journal of the International Mammalian Genome Society · 2018Review
- Induction of Type I Interferon through a Noncanonical Toll-Like Receptor 7 Pathway during Yersinia pestis Infection.Infection and immunity · 2017Article
- Type I interferons in infectious disease.Nature reviews. Immunology · 2015Review
- Bacterial programming of host responses: coordination between type I interferon and cell death.Frontiers in microbiology · 2014Review
- The bacterial pathogen Listeria monocytogenes and the interferon family: type I, type II and type III interferons.Frontiers in cellular and infection microbiology · 2014Review
- Confounding roles for type I interferons during bacterial and viral pathogenesis.International immunology · 2013Review
- Type I IFN exhaustion is a host defence protecting against secondary bacterial infections.Scandinavian journal of immunology · 2013Review
- Intranasal prophylaxis with CpG oligodeoxynucleotide can protect against Yersinia pestis infection.Infection and immunity · 2013Article
- Early sensing of Yersinia pestis airway infection by bone marrow cells.Frontiers in cellular and infection microbiology · 2012Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Type I interferons (IFN-I) broadly control innate immunity and are typically transcriptionally induced by Interferon Regulatory Factors (IRFs) following stimulation of pattern recognition receptors within the cytosol of host cells. For bacterial infection, IFN-I signaling can result in widely variant responses, in some cases contributing to the pathogenesis of disease while in others contributing to host defense. In this work, we addressed the role of type I IFN during Yersinia pestis infection in a murine model of septicemic plague. Transcription of IFN-β was induced in vitro and in vivo and contributed to pathogenesis. Mice lacking the IFN-I receptor, Ifnar, were less sensitive to disease and harbored more neutrophils in the later stage of infection which correlated with protection from lethality. In contrast, IRF-3, a transcription factor commonly involved in inducing IFN-β following bacterial infection, was not necessary for IFN production but instead contributed to host defense. In vitro, phagocytosis of Y. pestis by macrophages and neutrophils was more effective in the presence of IRF-3 and was not affected by IFN-β signaling. This activity correlated with limited bacterial growth in vivo in the presence of IRF-3. Together the data demonstrate that IRF-3 is able to activate pathways of innate immunity against bacterial infection that extend beyond regulation of IFN-β production.
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