ArticleMucosal immunology2013
A bacterial glycan core linked to surface (S)-layer proteins modulates host immunity through Th17 suppression.
Article in Mucosal immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 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
50 citing papers in PubMed, 83 citations in OpenAlex.
- Protein O-glycosylation in the Bacteroidota phylum.FEBS open bio · 2026Review
- Microbial Coaggregation in the Oral Cavity: Molecular Interactions and Current Insights.International journal of molecular sciences · 2025Review
- A new age in structural S-layer biology: Experimental and in silico milestones.The Journal of biological chemistry · 2025Review
- Oral bacterium contributes to periodontal inflammation by forming advanced glycation end products.Infection and immunity · 2025Article
- Microbiological and molecular aspects of periodontitis pathogenesis: an infection-induced inflammatory condition.Frontiers in cellular and infection microbiology · 2025Review
- Deciphering fucosylated protein-linked O-glycans in oral Tannerella serpentiformis: Insights from NMR spectroscopy and glycoproteomics.Glycobiology · 2024Article
- Pooled analysis of oral microbiome profiles defines robust signatures associated with periodontitis.mSystems · 2024Article
- Metatranscriptomic analysis shows functional alterations in subgingival biofilm in young smokers with periodontitis: a pilot study.Journal of applied oral science : revista FOB · 2024Observational
- The intriguing strategies ofFrontiers in oral health · 2024Article
- Oral microbiota-host interaction: the chief culprit of alveolar bone resorption.Frontiers in immunology · 2024Review
- The Roles of Periodontal Bacteria in Atherosclerosis.International journal of molecular sciences · 2023Review
- Multispecies biofilm behavior and host interaction support the association of Tannerella serpentiformis with periodontal health.Molecular oral microbiology · 2023Article
- S-layer proteins as immune players: Tales from pathogenic and non-pathogenic bacteria.Current research in microbial sciences · 2023Review
- Activation of bone marrow-derived dendritic cells and CD4Journal of oral microbiology · 2022Article
- Maintaining homeostatic control of periodontal bone tissue.Periodontology 2000 · 2021Review
- Taxonomic and Gene Category Analyses of Subgingival Plaques from a Group of Japanese Individuals with and without Periodontitis.International journal of molecular sciences · 2021Article
- Uncovering the Oral Dysbiotic Microbiota as Masters of Neutrophil Responses in the Pathobiology of Periodontitis.Frontiers in microbiology · 2021Review
- Nonulosonic acids contribute to the pathogenicity of the oral bacteriumInterface focus · 2019Review
- Chronic Inflammation as a Link between Periodontitis and Carcinogenesis.Mediators of inflammation · 2019Review
- Tannerella forsythia-produced methylglyoxal causes accumulation of advanced glycation endproducts to trigger cytokine secretion in human monocytes.Molecular oral microbiology · 2018Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Tannerella forsythia is a pathogen implicated in periodontitis, an inflammatory disease of the tooth-supporting tissues often leading to tooth loss. This key periodontal pathogen is decorated with a unique glycan core O-glycosidically linked to the bacterium's proteinaceous surface (S)-layer lattice and other glycoproteins. Herein, we show that the terminal motif of this glycan core acts to modulate dendritic cell effector functions to suppress T-helper (Th)17 responses. In contrast to the wild-type bacterial strain, infection with a mutant strain lacking the complete S-layer glycan core induced robust Th17 and reduced periodontal bone loss in mice. Our findings demonstrate that surface glycosylation of this pathogen may act to ensure its persistence in the host likely through suppression of Th17 responses. In addition, our data suggest that the bacterium then induces the Toll-like receptor 2-Th2 inflammatory axis that has previously been shown to cause bone destruction. Our study provides a biological basis for pathogenesis and opens opportunities in exploiting bacterial glycans as therapeutic targets against periodontitis and a range of other infectious diseases.
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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.