ArticlePLoS pathogens2015
TLR3 signaling in macrophages is indispensable for the protective immunity of invariant natural killer T cells against enterovirus 71 infection.
Article in PLoS pathogens, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 36 citations in OpenAlex.
- Review
- Severe enterovirus A71 infection is associated with dysfunction of T cell immune response and alleviated by Astragaloside A.Virologica Sinica · 2025Article
- Blocking CCL3-mediated neutrophil recruitment into the brain alleviates immunopathology following severe enterovirus 71 infection.iScience · 2024Article
- Moderate Prenatal Alcohol Exposure Increases Toll-like Receptor Activity in Umbilical Cord Blood at Birth: A Pilot Study.International journal of molecular sciences · 2024Article
- Virus-Triggered Autoimmunity Was Associated With Hirschsprung's Disease Through Activation of Innate Immunity.Journal of immunology research · 2024Article
- Review
- Human iNKT Cells Modulate Macrophage Survival and Phenotype.Biomedicines · 2022Article
- The iNKT Cell-Macrophage Axis in Homeostasis and Disease.International journal of molecular sciences · 2022Review
- Enterovirus D68 Protease 2AJournal of virology · 2021Article
- Human Antibodies to VP4 Inhibit Replication of Enteroviruses Across Subgenotypes and Serotypes, and Enhance Host Innate Immunity.Frontiers in microbiology · 2020Article
- Interplays between Enterovirus A71 and the innate immune system.Journal of biomedical science · 2019Review
- EV71 infection induces neurodegeneration via activating TLR7 signaling and IL-6 production.PLoS pathogens · 2019Article
- Toll-Like Receptor 3 Is Involved in Detection of Enterovirus A71 Infection and Targeted by Viral 2A Protease.Viruses · 2018Article
- Antiviral and Inflammatory Cellular Signaling Associated with Enterovirus 71 Infection.Viruses · 2018Review
- HRS plays an important role for TLR7 signaling to orchestrate inflammation and innate immunity upon EV71 infection.PLoS pathogens · 2017Article
- Enterovirus 71 3C Promotes Apoptosis through Cleavage of PinX1, a Telomere Binding Protein.Journal of virology · 2017Article
- Review
- Type I Interferons Triggered through the Toll-Like Receptor 3-TRIF Pathway Control Coxsackievirus A16 Infection in Young Mice.Journal of virology · 2015Article
- Innate-like lymphocytes in intestinal infections.Current opinion in infectious diseases · 2015Review
- iNKT Cells and Their Potential Lipid Ligands during Viral Infection.Frontiers in immunology · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
22 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Enterovirus 71 (EV71) is the most virulent pathogen among enteroviruses that cause hand, foot and mouth disease in children but rarely in adults. The mechanisms that determine the age-dependent susceptibility remain largely unclear. Here, we found that the paucity of invariant natural killer T (iNKT) cells together with immaturity of the immune system was related to the susceptibility of neonatal mice to EV71 infection. iNKT cells were crucial antiviral effector cells to protect young mice from EV71 infection before their adaptive immune systems were fully mature. EV71 infection led to activation of iNKT cells depending on signaling through TLR3 but not other TLRs. Surprisingly, iNKT cell activation during EV71 infection required TLR3 signaling in macrophages, but not in dendritic cells (DCs). Mechanistically, interleukin (IL)-12 and endogenous CD1d-restricted antigens were both required for full activation of iNKT cells. Furthermore, CD1d-deficiency led to dramatically increased viral loads in central nervous system and more severe disease in EV71-infected mice. Altogether, our results suggest that iNKT cells may be involved in controlling EV71 infection in children when their adaptive immune systems are not fully developed, and also imply that iNKT cells might be an intervention target for treating EV71-infected patients.
Indexed as
Identifiers
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.