ArticlePloS one2014
Differential induction of TLR3-dependent innate immune signaling by closely related parasite species.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
45 citing papers in PubMed, 72 citations in OpenAlex.
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- Mitochondrial damage and IL-1β production in monocytes caused byFrontiers in immunology · 2025Article
- Mutual regulations betweenFrontiers in immunology · 2024Review
- The Complexity of Interferon Signaling in Host Defense against Protozoan Parasite Infection.Pathogens (Basel, Switzerland) · 2023Review
- A genetic screen identifies a protective type III interferon response to Cryptosporidium that requires TLR3 dependent recognition.PLoS pathogens · 2022Article
- Inhibitor of growth protein 3 epigenetically silences endogenous retroviral elements and prevents innate immune activation.Nucleic acids research · 2021Article
- Neurological Infection, Kynurenine Pathway, and Parasitic Infection byFrontiers in immunology · 2021Review
- The Protective Role of TLR2 Mediates Impaired Autophagic Flux by Activating the mTOR Pathway DuringFrontiers in cellular and infection microbiology · 2021Article
- ROS-mediated NLRP3 inflammasome activation participates in the response against Neospora caninum infection.Parasites & vectors · 2020Article
- Impact ofPathogens (Basel, Switzerland) · 2020Article
- Neospora caninum infection induces an isolate virulence-dependent pro-inflammatory gene expression profile in bovine monocyte-derived macrophages.Parasites & vectors · 2020Article
- From Signaling Pathways to Distinct Immune Responses: Key Factors for Establishing or CombatingPathogens (Basel, Switzerland) · 2020Review
- Cell type- and species-specific host responses to Toxoplasma gondii and its near relatives.International journal for parasitology · 2020Review
- Immediate Interferon Gamma Induction Determines Murine Host Compatibility Differences between Toxoplasma gondii and Neospora caninum.Infection and immunity · 2020Article
- Activation of mosquito immunity blocks the development of transmission-stage filarial nematodes.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Interplay Between Reactive Oxygen Species and the Inflammasome Are Crucial for Restriction ofFrontiers in cellular and infection microbiology · 2020Article
- The Roles of Type I Interferon in Co-infections With Parasites and Viruses, Bacteria, or Other Parasites.Frontiers in immunology · 2020Review
- Article
- Toll-Like Receptor 3-TRIF Pathway Activation byInfection and immunity · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
The closely related protozoan parasites Toxoplasma gondii and Neospora caninum display similar life cycles, subcellular ultrastructure, invasion mechanisms, metabolic pathways, and genome organization, but differ in their host range and disease pathogenesis. Type II (γ) interferon has long been known to be the major mediator of innate and adaptive immunity to Toxoplasma infection, but genome-wide expression profiling of infected host cells indicates that Neospora is a potent activator of the type I (α/β) interferon pathways typically associated with antiviral responses. Infection of macrophages from mice with targeted deletions in various innate sensing genes demonstrates that host responses to Neospora are dependent on the toll-like receptor Tlr3 and the adapter protein Trif. Consistent with this observation, RNA from Neospora elicits TLR3-dependent type I interferon responses when targeted to the host endo-lysosomal system. Although live Toxoplasma fail to induce type I interferon, heat-killed parasites do trigger this response, albeit much weaker than Neospora, and co-infection studies reveal that T. gondii actively suppresses the production of type I interferon. These findings reveal that eukaryotic pathogens can be potent inducers of type I interferon and that related parasite species interact with this pathway in distinct ways.
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What OpenQuestion holds
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.