ArticleInfection and immunity2016
Primary Role for Toll-Like Receptor-Driven Tumor Necrosis Factor Rather than Cytosolic Immune Detection in Restricting Coxiella burnetii Phase II Replication within Mouse Macrophages.
Article in Infection and immunity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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.
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Who cites it
25 citing papers in PubMed, 31 citations in OpenAlex.
- TGF-β/IFN-γ Antagonism in Subversion and Self-Defense of Phase II Coxiella burnetiiInfection and immunity · 2023Trial
- Article
- The lipid A acylation pattern of Coxiella burnetii prevents detection and clearance by the non-canonical inflammasome in primary murine macrophages.PLoS pathogens · 2026Article
- Modulation of host cell pathways bymLife · 2025Review
- Obligate intracellular bacteria and host cell death pathways-the matter of life and death.Cell and tissue research · 2025Review
- Coxiella burnetii as a model system for understanding host immune response against obligate intracellular, vacuolar pathogens.PLoS pathogens · 2025Article
- Host Genetic Factors in Q Fever Susceptibility.Pathogens (Basel, Switzerland) · 2025Article
- Caspase-8 activity mediates TNFα production and restrictsInfection and immunity · 2024Article
- STING dependent BAX-IRF3 signaling results in apoptosis during late-stage Coxiella burnetii infection.Cell death & disease · 2024Article
- Caspase-8 activity mediates TNFα production and restrictsbioRxiv : the preprint server for biology · 2024Article
- TheProceedings of the National Academy of Sciences of the United States of America · 2023Article
- Bovine blood derived macrophages are unable to controlFrontiers in immunology · 2023Article
- Primary Murine Macrophages as a Tool for Virulence Factor Discovery in Coxiella burnetii.Microbiology spectrum · 2022Article
- To die or not to die: Programmed cell death responses and their interactions with Coxiella burnetii infection.Molecular microbiology · 2022Article
- Pattern Recognition Receptors in Innate Immunity to Obligate Intracellular Bacteria.Zoonoses (Shannon, Ireland) · 2021Article
- Recent Advances on the Innate Immune Response toFrontiers in cellular and infection microbiology · 2021Review
- MyD88 Is Required for Efficient Control ofFrontiers in immunology · 2019Article
- Coxiella burnetii Blocks Intracellular Interleukin-17 Signaling in Macrophages.Infection and immunity · 2018Article
- IRAK4 activity controls immune responses to intracellular bacteria Listeria monocytogenes and Mycobacterium smegmatis.Journal of leukocyte biology · 2018Article
- Host and Bacterial Factors Control Susceptibility of Drosophila melanogaster to Coxiella burnetii Infection.Infection and immunity · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
Coxiella burnetii replicates within permissive host cells by employing a Dot/Icm type IV secretion system (T4SS) to translocate effector proteins that direct the formation of a parasitophorous vacuole. C57BL/6 mouse macrophages restrict the intracellular replication of the C. burnetii. Nine Mile phase II (NMII) strain. However, eliminating Toll-like receptor 2 (TLR2) permits bacterial replication, indicating that the restriction of bacterial replication is immune mediated. Here, we examined whether additional innate immune pathways are employed by C57BL/6 macrophages to sense and restrict NMII replication. In addition to the known role of TLR2 in detecting and restricting NMII infection, we found that TLR4 also contributes to cytokine responses but is not required to restrict bacterial replication. Furthermore, the TLR signaling adaptors MyD88 and Trif are required for cytokine responses and restricting bacterial replication. The C. burnetii NMII T4SS translocates bacterial products into C57BL/6 macrophages. However, there was little evidence of cytosolic immune sensing of NMII, as there was a lack of inflammasome activation, T4SS-dependent cytokine responses, and robust type I interferon (IFN) production, and these pathways were not required to restrict bacterial replication. Instead, endogenous tumor necrosis factor (TNF) produced upon TLR sensing of C. burnetii NMII was required to control bacterial replication. Therefore, our findings indicate a primary role for TNF produced upon immune detection of C. burnetii NMII by TLRs, rather than cytosolic PRRs, in enabling C57BL/6 macrophages to restrict bacterial replication.
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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.