ArticleInfection and immunity2005
Mucosal FOXP3-expressing CD4+ CD25high regulatory T cells in Helicobacter pylori-infected patients.
Article in Infection and immunity, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 126 papers.
What it found
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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
126 citing papers in PubMed, 268 citations in OpenAlex.
- Messenger RNA expression of IL-8, FOXP3, and IL-12beta differentiates latent tuberculosis infection from disease.Journal of immunology (Baltimore, Md. : 1950) · 2007Trial
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- Inability of a fusion protein of IL-2 and diphtheria toxin (Denileukin Diftitox, DAB389IL-2, ONTAK) to eliminate regulatory T lymphocytes in patients with melanoma.Journal of immunotherapy (Hagerstown, Md. : 1997)Trial
- Design and Screening of the Peptide SAMP-12aa Derived from LL-37, Which Exhibits Anti-Molecules (Basel, Switzerland) · 2026Article
- Managing dangerous liaisons: lessons fromJournal of bacteriology · 2026Review
- Effects of Helicobacter pylori infection on T cell activation markers and regulatory T cells in people with and without HIV infection in Central Ethiopia.European journal of medical research · 2026Article
- Immunokinetic signatures ofFrontiers in cellular and infection microbiology · 2026Review
- Review
- Regulatory T cells and their role in allergic disease.Allergy · 2025Review
- T lymphocyte‑related immune response and immunotherapy in gastric cancer (Review).Oncology letters · 2024Review
- γδ T cells in human colon adenocarcinomas comprise mainly Vδ1, Vδ2, and Vδ3 cells with distinct phenotype and function.Cancer immunology, immunotherapy : CII · 2024Article
- Microbes little helpers and suppliers for therapeutic asthma approaches.Respiratory research · 2024Review
- Review
- Evolutionary Aspects of Diverse Microbial Exposures and Mental Health: Focus on "Old Friends" and Stress Resilience.Current topics in behavioral neurosciences · 2023Article
- Linking dysbiosis to precancerous stomach through inflammation: Deeper than and beyond imaging.Frontiers in immunology · 2023Review
- Construction of anoikis-related lncRNAs risk model: Predicts prognosis and immunotherapy response for gastric adenocarcinoma patients.Frontiers in pharmacology · 2023Article
- Article
- Article
- Immunological Perspective:Mediators of inflammation · 2022Review
- Intratumoral regulatory T cells from colon cancer patients comprise several activated effector populations.BMC immunology · 2021Article
66 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Helicobacter pylori chronically colonizes the stomach and duodenum and causes peptic ulcers or gastric adenocarcinoma in 10 to 20% of infected individuals. We hypothesize that the inability of patients to clear H. pylori infections is a consequence of active suppression of the immune response. Here we show that H. pylori-infected individuals have increased frequencies of CD4(+) CD25(high) T cells in both the stomach and duodenal mucosa compared to uninfected controls. These cells have the phenotype of regulatory T cells, as they express FOXP3, a key gene for the development and function of regulatory T cells, as well as high levels of the cytotoxic T lymphocyte-associated antigen 4 (CTLA-4) protein. In contrast, mucosal CD4(+) CD25(low) and CD4(+) CD25(-) cells express little FOXP3 mRNA and low levels of the CTLA-4 protein. Mucosal CD4(+) CD25(high) T cells are present in individuals with asymptomatic H. pylori infections as well as in duodenal ulcer patients. The frequencies of CD4(+) CD25(high) cells are also increased in the stomachs of H. pylori-infected patients with gastric adenocarcinoma, particularly in cancer-affected tissues. These findings suggest that regulatory T cells may suppress mucosal immune responses and thereby contribute to the persistence of H. pylori infections.
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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.