ArticleInfection and immunity2011
Role of gastric epithelial cell-derived transforming growth factor beta in reduced CD4+ T cell proliferation and development of regulatory T cells during Helicobacter pylori infection.
Article in Infection and immunity, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
23 citing papers in PubMed, 51 citations in OpenAlex.
- TGF-β signaling in health, disease, and therapeutics.Signal transduction and targeted therapy · 2024Review
- Regulation of regulatory T cells and tumor-associated macrophages in gastric cancer tumor microenvironment.Cancer medicine · 2024Review
- Review
- Article
- The Efficacy of Cancer Immunotherapies Is Compromised byFrontiers in immunology · 2022Review
- Crosstalk of Microorganisms and Immune Responses in Autoimmune Neuroinflammation: A Focus on Regulatory T Cells.Frontiers in immunology · 2021Review
- Altered cytokine expression in Helicobacter pylori infected patients with bleeding duodenal ulcer.BMC research notes · 2019Article
- Article
- Helicobacter pylori Deregulates T and B Cell Signaling to Trigger Immune Evasion.Current topics in microbiology and immunology · 2019Review
- Regulation of the Immune Response by TGF-β: From Conception to Autoimmunity and Infection.Cold Spring Harbor perspectives in biology · 2017Review
- Anti-Helicobacter pylori activity of crude N-acetylneuraminic acid isolated from glycomacropeptide of whey.Laboratory animal research · 2016Article
- Thrombospondin-1-dependent immune regulation by transforming growth factor-β2-exposed antigen-presenting cells.Immunology · 2015Article
- Influence of TGFB1 C-509T polymorphism on gastric cancer risk associated with TGF-β1 expression in the gastric mucosa.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2015Article
- Upregulation of miR-142-5p in atherosclerotic plaques and regulation of oxidized low-density lipoprotein-induced apoptosis in macrophages.Molecular medicine reports · 2015Article
- Transforming growth factor-β: an important mediator in Helicobacter pylori-associated pathogenesis.Frontiers in cellular and infection microbiology · 2015Review
- Regulatory T-Cells at the Interface between Human Host and Pathogens in Infectious Diseases and Vaccination.Frontiers in immunology · 2015Review
- Smad2 is involved in Aggregatibacter actinomycetemcomitans-induced apoptosis.Journal of dental research · 2014Article
- Article
- CagA-dependent downregulation of B7-H2 expression on gastric mucosa and inhibition of Th17 responses during Helicobacter pylori infection.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- Stromal cells induce Th17 during Helicobacter pylori infection and in the gastric tumor microenvironment.PloS one · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Gastric epithelial cells (GECs) express the class II major histocompatibility complex (MHC) and costimulatory molecules, enabling them to act as antigen-presenting cells (APCs) and affect local T cell responses. During Helicobacter pylori infection, GECs respond by releasing proinflammatory cytokines and by increasing the surface expression of immunologically relevant receptors, including class II MHC. The CD4(+) T cell response during H. pylori infection is skewed toward a Th1 response, but these cells remain hyporesponsive. Activated T cells show decreased proliferation during H. pylori infection, and CD4(+) CD25(+) FoxP3(+) regulatory T cells (Tregs) are present at the site of infection. In this study, we examined the mechanisms surrounding the CD4(+) T cell responses during H. pylori infection and found that transforming growth factor β (TGF-β) plays a major role in these responses. GECs produced TGF-β1 and TGF-β2 in response to infection. Activated CD4(+) T cells in culture with H. pylori-treated GECs were decreased in proliferation but increased upon neutralization of TGF-β. Naïve CD4(+) T cell development into Tregs was also enhanced in the presence of GEC-derived TGF-β. Herein, we demonstrate a role for GEC-produced TGF-β in the inhibition of CD4(+) T cell responses seen during H. pylori infection.
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What OpenQuestion holds
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.