ArticlePloS one2013
MyD88 deficiency markedly worsens tissue inflammation and bacterial clearance in mice infected with Treponema pallidum, the agent of syphilis.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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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
12 citing papers in PubMed, 21 citations in OpenAlex.
- TheJornal brasileiro de doencas sexualmente transmissiveis : DST · 2026Article
- Development and utilization ofmBio · 2025Article
- Research Advances in Clinical Strategies and Preclinical Models for Syphilis Relapse.Infection and drug resistance · 2025Review
- Immunodominant extracellular loops of Treponema pallidum FadL outer membrane proteins elicit antibodies with opsonic and growth-inhibitory activities.PLoS pathogens · 2024Article
- Development and utilization ofbioRxiv : the preprint server for biology · 2024Article
- Immunodominant extracellular loops ofbioRxiv : the preprint server for biology · 2024Article
- Use of Epivolve phage display to generate a monoclonal antibody with opsonic activity directed against a subdominant epitope on extracellular loop 4 ofFrontiers in immunology · 2023Article
- MiR-223-3p inhibits rTp17-induced inflammasome activation and pyroptosis by targeting NLRP3.Journal of cellular and molecular medicine · 2020Article
- Characterization ofFrontiers in immunology · 2020Article
- Syphilis Reactivates Latent Epstein-Barr Virus Reservoir via Toll-Like Receptor 2 and B-Cell Receptor Activation.Open forum infectious diseases · 2019Article
- Syphilis.Nature reviews. Disease primers · 2017Review
- Treponema pallidum, the syphilis spirochete: making a living as a stealth pathogen.Nature reviews. Microbiology · 2016Review
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
Research on syphilis, a sexually transmitted infection caused by the non-cultivatable spirochete Treponema pallidum, has been hampered by the lack of an inbred animal model. We hypothesized that Toll-like receptor (TLR)-dependent responses are essential for clearance of T. pallidum and, consequently, compared infection in wild-type (WT) mice and animals lacking MyD88, the adaptor molecule required for signaling by most TLRs. MyD88-deficient mice had significantly higher pathogen burdens and more extensive inflammation than control animals. Whereas tissue infiltrates in WT mice consisted of mixed mononuclear and plasma cells, infiltrates in MyD88-deficient animals were predominantly neutrophilic. Although both WT and MyD88-deficient mice produced antibodies that promoted uptake of treponemes by WT macrophages, MyD88-deficient macrophages were deficient in opsonophagocytosis of treponemes. Our results demonstrate that TLR-mediated responses are major contributors to the resistance of mice to syphilitic disease and that MyD88 signaling and FcR-mediated opsonophagocytosis are linked to the macrophage-mediated clearance of treponemes.
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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.