ArticleGastroenterology2011
Tolerance rather than immunity protects from Helicobacter pylori-induced gastric preneoplasia.
Article in Gastroenterology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 181 papers, 2 of them syntheses that pooled it.
What it found
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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
181 citing papers in PubMed, 2 syntheses or guidelines pooled it, 291 citations in OpenAlex.
- Is Helicobacter pylori Infection Associated with Celiac Disease? A Meta-analysis.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2022Pooled it
- Association Between Helicobacter pylori Exposure and Decreased Odds of Eosinophilic Esophagitis-A Systematic Review and Meta-analysis.Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association · 2019Pooled it
- Chestnut (Castanea sativa Mill.) leaf extract and pure castalagin reduce bacterial colonisation and the associated inflammation in gastric organoids and a mouse model of H. pylori infection.Inflammopharmacology · 2026Article
- Bad bugs mean business: gastric cancer is an intended consequence ofInfection and immunity · 2026Review
- Diet-Induced Obesity ExacerbatesbioRxiv : the preprint server for biology · 2026Article
- Outer Membrane Vesicles Mediate the Secretion and Nuclear Trafficking of a Bacterial Nucleomodulin.Journal of extracellular vesicles · 2026Article
- Immunomodulatory Role of Milk on Gut Microbiota: Implications for Enhancing Oral Vaccine Efficacy.Probiotics and antimicrobial proteins · 2026Review
- Managing dangerous liaisons: lessons fromJournal of bacteriology · 2026Review
- Therapeutic suppression ofFrontiers in microbiology · 2026Article
- Targeting regulatory T cell plasticity in gastric cancer: a unified bimodal model and precision immunotherapy paradigm: a hypothesis-generating review.Frontiers in oncology · 2026Article
- Metaplasia Enables Stomach Colonization bybioRxiv : the preprint server for biology · 2025Article
- Salmonella-superspreader hosts require gut regulatory T cells to maintain a disease-tolerant state.The Journal of experimental medicine · 2025Article
- Research advancements and evaluation of multifactor-induced murine models for gastric cancer.Animal models and experimental medicine · 2025Review
- Neonatal infection withInfection and immunity · 2025Article
- ARID1A mutation drives gastric tumorigenesis via activating type 2 immune dominant microenvironment.iScience · 2025Article
- Genetic Basis of Gap Formation Between MigratingMicroorganisms · 2025Article
- An affinity-based depletion strategy for evaluating the effects of ergothioneine on bacterial physiology.Cell chemical biology · 2025Article
- Immuno-neural mechanisms in gastrointestinal tumorigenesis: bridging inflammation, neural regulation, and therapeutic innovation.Frontiers in immunology · 2025Review
- A critical review onFrontiers in cellular and infection microbiology · 2025Review
- Gut microbiota and healthy longevity.Science China. Life sciences · 2024Review
121 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 5 institutions in 3 countries.
Funding
Abstract
BACKGROUND &
aimsChronic infection with the bacterial pathogen Helicobacter pylori causes gastric disorders, ranging from chronic gastritis to gastric adenocarcinoma. Only a subset of infected persons will develop overt disease; most remains asymptomatic despite lifelong colonization. This study aims to elucidate the differential susceptibility to H pylori that is found both across and within populations.
methodsWe have established a C57BL/6 mouse model of H pylori infection with a strain that is capable of delivering the virulence factor cytotoxin-associated gene A (CagA) into host cells through the activity of a Cag-pathogenicity island-encoded type IV secretion system.
resultsMice infected at 5-6 weeks of age with CagA(+)H pylori rapidly develop gastritis, gastric atrophy, epithelial hyperplasia, and metaplasia in a type IV secretion system-dependent manner. In contrast, mice infected during the neonatal period with the same strain are protected from preneoplastic lesions. Their protection results from the development of H pylori-specific peripheral immunologic tolerance, which requires transforming growth factor-β signaling and is mediated by long-lived, inducible regulatory T cells, and which controls the local CD4(+) T-cell responses that trigger premalignant transformation. Tolerance to H pylori develops in the neonatal period because of a biased ratio of T-regulatory to T-effector cells and is favored by prolonged low-dose exposure to antigen.
conclusionsUsing a novel CagA(+)H pylori infection model, we report here that the development of tolerance to H pylori protects from gastric cancer precursor lesions. The age at initial infection may thus account for the differential susceptibility of infected persons to H pylori-associated disease manifestations.
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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.