ArticleInfection and immunity2013
TRIF mediates Toll-like receptor 2-dependent inflammatory responses to Borrelia burgdorferi.
Article in Infection and immunity, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 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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Who cites it
44 citing papers in PubMed, 60 citations in OpenAlex.
- Endosome restricted human TLR1 polymorphism highlights a role for MyD88 in Pam3CSK4 detection.PloS one · 2026Article
- The role of inflammatory gene polymorphisms in severe COVID-19: a review.Virology journal · 2024Review
- Molecular Mechanisms of Cachexia: A Review.Cells · 2024Review
- Borrelia burgdorferi initiates early transcriptional re-programming in macrophages that supports long-term suppression of inflammation.PLoS pathogens · 2023Article
- Single-cell RNA sequencing of murine ankle joints over time reveals distinct transcriptional changes followingiScience · 2023Article
- Review
- Croquemort elicits activation of the immune deficiency pathway in ticks.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Comparative transcriptome analysis ofFrontiers in cellular and infection microbiology · 2023Article
- An AP-3-dependent pathway directs phagosome fusion with Rab8 and Rab11 vesicles involved in TLR2 signaling.Traffic (Copenhagen, Denmark) · 2022Article
- Macrophage mediated recognition and clearance of Borrelia burgdorferi elicits MyD88-dependent and -independent phagosomal signals that contribute to phagocytosis and inflammation.BMC immunology · 2021Article
- A murine model of Lyme disease demonstrates that Borrelia burgdorferi colonizes the dura mater and induces inflammation in the central nervous system.PLoS pathogens · 2021Article
- Immune Response toCurrent issues in molecular biology · 2021Article
- Recent Progress in Lyme Disease and Remaining Challenges.Frontiers in medicine · 2021Review
- The Lyme disease bacterium, Borrelia burgdorferi, stimulates an inflammatory response in human choroid plexus epithelial cells.PloS one · 2020Article
- Beyond defense: regulation of neuronal morphogenesis and brain functions via Toll-like receptors.Journal of biomedical science · 2019Review
- Regulation of macrophage activity by surface receptors contained within Borrelia burgdorferi-enriched phagosomal fractions.PLoS pathogens · 2019Article
- The outer membrane protein Tp92 of Treponema pallidum induces human mononuclear cell death and IL-8 secretion.Journal of cellular and molecular medicine · 2018Article
- TRIF is a key inflammatory mediator of acute sickness behavior and cancer cachexia.Brain, behavior, and immunity · 2018Article
- A multi-omic analysis reveals the regulatory role of CD180 during the response of macrophages to Borrelia burgdorferi.Emerging microbes & infections · 2018Article
- Primary Human Microglia Are Phagocytically Active and Respond toFrontiers in microbiology · 2018Article
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
TRIF is an adaptor molecule important in transducing signals from intracellularly signaling Toll-like receptor 3 (TLR3) and TLR4. Recently, TLR2 was found to signal from intracellular compartments. Using a synthetic ligand for TLR2/1 heterodimers, as well as Borrelia burgdorferi, which is a strong activator of TLR2/1, we found that TLR2 signaling can utilize TRIF. Unlike TRIF signaling by other TLRs, TLR2-mediated TRIF signaling is dependent on the presence of another adaptor molecule, MyD88. However, unlike MyD88 deficiency, TRIF deficiency does not result in diminished control of infection with B. burgdorferi in a murine model of disease. This appears to be due to the effects of MyD88 on phagocytosis via scavenger receptors, such as MARCO, which are not affected by the loss of TRIF. In mice, TRIF deficiency did have an effect on the production of inflammatory cytokines, suggesting that regulation of inflammatory cytokines and control of bacterial growth may be uncoupled, in part through transduction of TLR2 signaling through TRIF.
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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.