ArticlePLoS pathogens2015
Induction of interferon-stimulated genes by IRF3 promotes replication of Toxoplasma gondii.
Article in PLoS pathogens, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 21 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
21 citing papers in PubMed, 34 citations in OpenAlex.
- Retraction: Induction of Interferon-Stimulated Genes by IRF3 Promotes Replication of Toxoplasma gondii.PLoS pathogens · 2024Article
- TRIM56-mediated production of type I interferon inhibits intracellular replication ofMicrobiology spectrum · 2024Article
- Comparative characterization of microRNA-71 of Echinococcus granulosus exosomes.Parasite (Paris, France) · 2023Article
- Function and regulation of cGAS-STING signaling in infectious diseases.Frontiers in immunology · 2023Review
- Multifaceted functions of STING in human health and disease: from molecular mechanism to targeted strategy.Signal transduction and targeted therapy · 2022Review
- Article
- IRF3 inhibits IFN-γ-mediated restriction of intracellular pathogens in macrophages independently of IFNAR.Journal of leukocyte biology · 2022Article
- cGAS exacerbates Schistosoma japonicum infection in a STING-type I IFN-dependent and independent manner.PLoS pathogens · 2022Article
- Leishmania kinetoplast DNA contributes to parasite burden in infected macrophages: Critical role of the cGAS-STING-TBK1 signaling pathway in macrophage parasitemia.Frontiers in immunology · 2022Article
- FAF1 downregulation by Toxoplasma gondii enables host IRF3 mobilization and promotes parasite growth.Journal of cellular and molecular medicine · 2021Article
- The role of the adaptor molecule STING during Schistosoma mansoni infection.Scientific reports · 2020Article
- RIG-I Has a Role in Immunity AgainstFrontiers in immunology · 2020Article
- Research Advances in How the cGAS-STING Pathway Controls the Cellular Inflammatory Response.Frontiers in immunology · 2020Review
- The cGAS-STING Pathway in Hematopoiesis and Its Physiopathological Significance.Frontiers in immunology · 2020Review
- The GRA15 protein fromThe Journal of biological chemistry · 2019Article
- Tryptophan-kynurenine pathway attenuates β-catenin-dependent pro-parasitic role of STING-TICAM2-IRF3-IDO1 signalosome in Toxoplasma gondii infection.Cell death & disease · 2019Article
- Malaria parasite DNA-harbouring vesicles activate cytosolic immune sensors.Nature communications · 2017Article
- The nonstructural proteins of Pneumoviruses are remarkably distinct in substrate diversity and specificity.Virology journal · 2017Article
- No TRIFling Matter on STING.Cell host & microbe · 2016Article
- STING Requires the Adaptor TRIF to Trigger Innate Immune Responses to Microbial Infection.Cell host & microbe · 2016Article
Corrections and comments
- Retraction · 2024-05-31Concerns/Issues about Results and/or Conclusions · Duplication of/in Image · Error in Image · Euphemisms for Duplication · Investigation by Journal/Publisher · Investigation by Third Party · Objections by Author(s) · Original Data and/or Images not Provided and/or not Available · Unreliable Results and/or Conclusions · · see also: https://pubpeer.com/publications/41DF0E615F9FC5F814FE96A02B87FA
- Retracted
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Innate immunity is the first line of defense against microbial insult. The transcription factor, IRF3, is needed by mammalian cells to mount innate immune responses against many microbes, especially viruses. IRF3 remains inactive in the cytoplasm of uninfected cells; upon virus infection, it gets phosphorylated and then translocates to the nucleus, where it binds to the promoters of antiviral genes and induces their expression. Such genes include type I interferons (IFNs) as well as Interferon Stimulated Genes (ISGs). IRF3-/- cells support enhanced replication of many viruses and therefore, the corresponding mice are highly susceptible to viral pathogenesis. Here, we provide evidence for an unexpected pro-microbial role of IRF3: the replication of the protozoan parasite, Toxoplasma gondii, was significantly impaired in IRF3-/- cells. In exploring whether the transcriptional activity of IRF3 was important for its pro-parasitic function, we found that ISGs induced by parasite-activated IRF3 were indeed essential, whereas type I interferons were not important. To delineate the signaling pathway that activates IRF3 in response to parasite infection, we used genetically modified human and mouse cells. The pro-parasitic signaling pathway, which we termed PISA (Parasite-IRF3 Signaling Activation), activated IRF3 without any involvement of the Toll-like receptor or RIG-I-like receptor pathways, thereby ruling out a role of parasite-derived RNA species in activating PISA. Instead, PISA needed the presence of cGAS, STING, TBK1 and IRF3, indicating the necessity of DNA-triggered signaling. To evaluate the physiological significance of our in vitro findings, IRF3-/- mice were challenged with parasite infection and their morbidity and mortality were measured. Unlike WT mice, the IRF3-/- mice did not support replication of the parasite and were resistant to pathogenesis caused by it. Our results revealed a new paradigm in which the antiviral host factor, IRF3, plays a cell-intrinsic pro-parasitic role.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.