ArticleNature communications2019
T4SS-dependent TLR5 activation by Helicobacter pylori infection.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 82 citations in OpenAlex.
- Innate immunity: current understandings and future perspectives.Signal transduction and targeted therapy · 2026Review
- Immunoinformatic-driven design of a multi-epitope vaccine againstBiochemistry and biophysics reports · 2026Article
- Enhanced ADP-heptose-dependent NF-κB activation bymicroLife · 2026Article
- A Narrative Review on Unravelling Bacterial-Mediated Carcinogenesis and Possible Alternative Treatment Strategies.BioMed research international · 2026Review
- Pathogenicity and virulence ofVirulence · 2025Review
- Molecular characterization of fourGut microbes · 2025Article
- Serological and virological characterization of hepatitis B surface antigen-positive patients with or without Helicobacter pylori co-infection at the university of Gondar comprehensive specialized hospital, Northwest Ethiopia.BMC infectious diseases · 2025Article
- Clinical and biochemical characterization of hepatitis B surface antigen-positive patients with or withoutFrontiers in immunology · 2025Article
- The Influence of Gastric Microbiota and Probiotics inBiomedicines · 2024Review
- Cultivation and molecular characterization of viable Helicobacter pylori from the root canal of 170 deciduous teeth of children.Cell communication and signaling : CCS · 2024Article
- Developing a potent vaccine againstExpert reviews in molecular medicine · 2024Review
- Current Knowledge about Gastric Microbiota with Special Emphasis onCurrent issues in molecular biology · 2024Review
- Sustained exposure to Helicobacter pylori induces immune tolerance by desensitizing TLR6.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2024Article
- New Promising Routes in Peptic Ulcers: Toll-like Receptors and Semaphorins.Endocrine, metabolic & immune disorders drug targets · 2024Review
- Current study of pathogenetic mechanisms and therapeutics of chronic atrophic gastritis: a comprehensive review.Frontiers in cell and developmental biology · 2024Review
- Common diagnostic biomarkers and molecular mechanisms ofFrontiers in immunology · 2024Article
- Designing and development of multi-epitope chimeric vaccine against Helicobacter pylori by exploring its entire immunogenic epitopes: an immunoinformatic approach.BMC bioinformatics · 2023Article
- The TLR/MyD88 signalling cascade in inflammation and gastric cancer: the immune regulatory network of Helicobacter pylori.Journal of molecular medicine (Berlin, Germany) · 2023Review
- Article
- Intersections between innate immune response and gastric cancer development.World journal of gastroenterology · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Toll-like receptor TLR5 recognizes a conserved domain, termed D1, that is present in flagellins of several pathogenic bacteria but not in Helicobacter pylori. Highly virulent H. pylori strains possess a type IV secretion system (T4SS) for delivery of virulence factors into gastric epithelial cells. Here, we show that one of the H. pylori T4SS components, protein CagL, can act as a flagellin-independent TLR5 activator. CagL contains a D1-like motif that mediates adherence to TLR5
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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.