ArticleThe Journal of experimental medicine2011
Host innate recognition of an intestinal bacterial pathogen induces TRIF-dependent protective immunity.
Article in The Journal of experimental medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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.
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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.
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Who cites it
34 citing papers in PubMed, 51 citations in OpenAlex.
- Deciphering the Implications ofPathogens (Basel, Switzerland) · 2026Review
- Unveiling the gut-liver axis: the behind-the-scenes "manipulator" of human immune function.Frontiers in immunology · 2025Review
- Type I interferons in bacterial diseases: myeloid cells at the crossroads of protection and pathology.Frontiers in immunology · 2025Review
- Pathogenicity and virulence ofVirulence · 2024Review
- Impact of Type I Interferons on Susceptibility to Bacterial Pathogens.Trends in microbiology · 2021Review
- Review
- The role of natural killer cells in Parkinson's disease.Experimental & molecular medicine · 2020Review
- Bacterial polyphosphates interfere with the innate host defense to infection.Nature communications · 2020Article
- Beyond IgE: Alternative Mast Cell Activation Across Different Disease States.International journal of molecular sciences · 2020Review
- Cell-line-based assay for the toxicity/benefit analysis of lipopolysaccharides in plants.Chemical biology & drug design · 2020Article
- Human Gut-Associated Natural Killer Cells in Health and Disease.Frontiers in immunology · 2019Review
- CD14Gut · 2018Article
- Selective autophagy of the adaptor TRIF regulates innate inflammatory signaling.Nature immunology · 2018Article
- Kinase Activities of RIPK1 and RIPK3 Can Direct IFN-β Synthesis Induced by Lipopolysaccharide.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- Article
- Type I and III Interferon in the Gut: Tight Balance between Host Protection and Immunopathology.Frontiers in immunology · 2017Review
- TIR-Domain-Containing Adapter-Inducing Interferon-Journal of clinical & cellular immunology · 2016Article
- Article
- Age-dependent variation in innate immune responses to porcine epidemic diarrhea virus infection in suckling versus weaned pigs.Veterinary immunology and immunopathology · 2015Article
- A Single Bacterial Immune Evasion Strategy Dismantles Both MyD88 and TRIF Signaling Pathways Downstream of TLR4.Cell host & microbe · 2015Article
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
Toll-like receptor 4 (TLR4), which signals through the adapter molecules myeloid differentiation factor 88 (MyD88) and toll/interleukin 1 receptor domain-containing adapter inducing IFN-β (TRIF), is required for protection against Gram-negative bacteria. TRIF is known to be important in TLR3-mediated antiviral signaling, but the role of TRIF signaling against Gram-negative enteropathogens is currently unknown. We show that TRIF signaling is indispensable for establishing innate protective immunity against Gram-negative Yersinia enterocolitica. Infection of wild-type mice rapidly induced both IFN-β and IFN-γ in the mesenteric lymph nodes. In contrast, TRIF-deficient mice were defective in these IFN responses and showed impaired phagocytosis in regional macrophages, resulting in greater bacterial dissemination and mortality. TRIF signaling may be universally important for protection against Gram-negative pathogens, as TRIF-deficient macrophages were also impaired in killing both Salmonella and Escherichia coli in vitro. The mechanism of TRIF-mediated protective immunity appears to be orchestrated by macrophage-induced IFN-β and NK cell production of IFN-γ. Sequential induction of IFN-β and IFN-γ leads to amplification of macrophage bactericidal activity sufficient to eliminate the invading pathogens at the intestinal interface. Our results demonstrate a previously unknown role of TRIF in host resistance to Gram-negative enteropathogens, which may lead to effective strategies for combating enteric infections.
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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.