ArticleInfection and immunity2013
Complex T cell interactions contribute to Helicobacter pylori gastritis in mice.
Article in Infection and immunity, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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.
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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
29 citing papers in PubMed, 60 citations in OpenAlex.
- Beyond the Stomach: Exploring the Role ofExpert reviews in molecular medicine · 2026Review
- Comparison of gastric inflammation and metaplasia induced byMicrobiology spectrum · 2024Article
- Effects ofFrontiers in cellular and infection microbiology · 2024Review
- Helicobacter pylori Chronic-Stage Inflammation Undergoes Fluctuations That Are Altered inInfection and immunity · 2023Article
- IL-17 Receptor Signaling through IL-17A or IL-17F Is Sufficient to Maintain Innate Response and Control ofImmunoHorizons · 2022Article
- Evaluating the relationship betweenAnnals of medicine and surgery (2012) · 2021Article
- NF-κB in Gastric Cancer Development and Therapy.Biomedicines · 2021Review
- Interleukin- 17agene Polymorphism, Serum Level and Its Tissue Expression in Iraqi Patients Gastric Lesions.Medical archives (Sarajevo, Bosnia and Herzegovina) · 2021Article
- Helicobacter pylori metabolites exacerbate gastritis through C-type lectin receptors.The Journal of experimental medicine · 2021Article
- Cytokine Profile of CCR6Sovremennye tekhnologii v meditsine · 2021Article
- Association between renal function and co-infection with Clonorchis sinensis and Helicobacter pylori: a cross-sectional study.BMC infectious diseases · 2020Article
- T Cell Cytokines Impact Epithelial Cell Responses duringJournal of immunology (Baltimore, Md. : 1950) · 2020Review
- Notch 1 Is Involved in CD4Frontiers in cellular and infection microbiology · 2020Article
- CD103 Promotes the Pro-inflammatory Response of Gastric Resident CD4Frontiers in cellular and infection microbiology · 2020Article
- Th17 Cells in Helicobacter pylori Infection: a Dichotomy of Help and Harm.Infection and immunity · 2019Review
- Article
- Nucleotide-binding oligomerization domain 1 andWorld journal of gastroenterology · 2018Review
- Strategies used byWorld journal of gastroenterology · 2017Review
- CagY Is an Immune-Sensitive Regulator of the Helicobacter pylori Type IV Secretion System.Gastroenterology · 2016Article
- Interferon-γ promotes gastric lymphoid follicle formation but not gastritis inGut pathogens · 2016Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Disease due to the gastric pathogen Helicobacter pylori varies in severity from asymptomatic to peptic ulcer disease and cancer. Accumulating evidence suggests that one source of this variation is an abnormal host response. The goal of this study was to use a mouse model of H. pylori gastritis to investigate the roles of regulatory T cells (Treg) as well as proinflammatory T cells (Th1 and Th17) in gastritis, gastric T cell engraftment, and gastric cytokine production. Our results support published data indicating that severe gastritis in T cell recipient mice is due to failure of Treg engraftment, that Treg ameliorate gastritis, and that the proinflammatory response is attributable to interactions between several cell subsets and cytokines. We confirmed that gamma interferon (IFN-γ) is essential for induction of gastritis but showed that IFN-γ-producing CD4 T cells are not necessary. Interleukin 17A (IL-17A) also contributed to gastritis, but to a lesser extent than IFN-γ. Tumor necrosis factor alpha (TNF-α) and IL-17F were also elevated in association with disease. These results indicate that while H. pylori-specific CD4(+) T cells and IFN-γ are both essential for induction of gastritis due to H. pylori, IFN-γ production by T cells is not essential. It is likely that other proinflammatory cytokines, such as IL-17F and TNF-α, shown to be elevated in this model, also contribute to the induction of disease. We suggest that gastritis due to H. pylori is associated with loss of immunoregulation and alteration of several cytokines and cell subsets and cannot be attributed to a single immune pathway.
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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.