ArticleJournal of immunology (Baltimore, Md. : 1950)2016
Cell-Extrinsic TNF Collaborates with TRIF Signaling To Promote Yersinia-Induced Apoptosis.
Article in Journal of immunology (Baltimore, Md. : 1950), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 48 citations in OpenAlex.
- PANoptosis in the pathogenesis of myelodysplastic syndromes.Molecular oncology · 2026Review
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- Pathogenicity and virulence ofVirulence · 2024Review
- Yersinia infection induces glucose depletion and AMPK-dependent inhibition of pyroptosis in mice.Nature microbiology · 2024Article
- Blockade of IKK signaling induces RIPK1-independent apoptosis in human macrophages.PLoS pathogens · 2024Article
- Distinct sequential death complexes regulate pyroptosis and IL-1β release in response toScience advances · 2024Article
- Differential signalling requirements for RIPK1-dependent pyroptosis in neutrophils and macrophages.Cell death & disease · 2024Article
- A TNF-IL-1 circuit controls Yersinia within intestinal pyogranulomas.The Journal of experimental medicine · 2024Article
- Apoptosis and its pathways as targets for intracellular pathogens to persist in cells.Parasitology research · 2023Review
- TNF licenses macrophages to undergo rapid caspase-1, -11, and -8-mediated cell death that restricts Legionella pneumophila infection.PLoS pathogens · 2023Article
- Death by TNF: a road to inflammation.Nature reviews. Immunology · 2023Review
- A TNF-IL-1 circuit controlsbioRxiv : the preprint server for biology · 2023Article
- Neutrophils and macrophages drive TNF-induced lethality via TRIF/CD14-mediated responses.Science immunology · 2022Article
- Macrophages in periodontitis: A dynamic shift between tissue destruction and repair.The Japanese dental science review · 2022Review
- Protective Effect of Levilactobacillus brevis Against Yersinia enterocolitica Infection in Mouse Model via Regulating MAPK and NF-κB Pathway.Probiotics and antimicrobial proteins · 2022Article
- Role of the Yersinia pseudotuberculosis Virulence Plasmid in Pathogen-Phagocyte Interactions in Mesenteric Lymph Nodes.EcoSal Plus · 2021Review
- Heightened Virulence ofInfection and immunity · 2021Article
- Genetic targeting of Card19 is linked to disrupted NINJ1 expression, impaired cell lysis, and increased susceptibility to Yersinia infection.PLoS pathogens · 2021Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Innate immune responses that are crucial for control of infection are often targeted by microbial pathogens. Blockade of NF-κB and MAPK signaling by the Yersinia virulence factor YopJ inhibits cytokine production by innate immune cells but also triggers cell death. This cell death requires RIPK1 kinase activity and caspase-8, which are engaged by TLR4 and the adaptor protein TRIF. Nevertheless, TLR4- and TRIF-deficient cells undergo significant apoptosis, implicating TLR4/TRIF-independent pathways in the death of Yersinia-infected cells. In this article, we report a key role for TNF/TNFR1 in Yersinia-induced cell death of murine macrophages, which occurs despite the blockade of NF-κB and MAPK signaling imposed by Yersinia on infected cells. Intriguingly, direct analysis of YopJ injection revealed a heterogeneous population of injection-high and injection-low cells, and demonstrated that TNF expression came from the injection-low population. Moreover, TNF production by this subpopulation was necessary for maximal apoptosis in the population of highly injected cells, and TNFR-deficient mice displayed enhanced susceptibility to Yersinia infection. These data demonstrate an important role for collaboration between TNF and pattern recognition receptor signals in promoting maximal apoptosis during bacterial infection, and demonstrate that heterogeneity in virulence factor injection and cellular responses play an important role in promoting anti-Yersinia immune defense.
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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.