ArticleInfection and immunity2000
Helicobacter pylori modulates lymphoepithelial cell interactions leading to epithelial cell damage through Fas/Fas ligand interactions.
Article in Infection and immunity, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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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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Who cites it
34 citing papers in PubMed, 111 citations in OpenAlex.
- Mitochondrial Stress inAntioxidants (Basel, Switzerland) · 2026Review
- miR-136: A biomarker in the inflammation-cancer transformation of gastric cancer.World journal of gastrointestinal oncology · 2025Article
- Historical and Molecular Perspectives on the Presence ofInternational journal of molecular sciences · 2024Review
- Isolation of lymphocytes from the human gastric mucosa.World journal of methodology · 2021Review
- Two Distinct Etiologies of Gastric Cancer: Infection and Autoimmunity.Frontiers in cell and developmental biology · 2021Review
- Gastric Cancer in the Era of Immune Checkpoint Blockade.Journal of oncology · 2019Review
- Helicobacter pylori outer membrane vesicles involvement in the infection development and Helicobacter pylori-related diseases.Journal of biomedical science · 2018Review
- Role of caspase-3/E-cadherin in helicobacter pylori-induced apoptosis of gastric epithelial cells.Oncotarget · 2017Article
- The Role of the Microbiome in Gastrointestinal Cancer.Gastroenterology clinics of North America · 2016Review
- Interferon-γ-producing B cells induce the formation of gastric lymphoid follicles after Helicobacter suis infection.Mucosal immunology · 2015Article
- Helicobacter pylori sensitizes TNF-related apoptosis-inducing ligand (TRAIL)-mediated apoptosis in human gastric epithelial cells through regulation of FLIP.Cell death & disease · 2014Article
- Neonatal Fc receptor for IgG (FcRn) expressed in the gastric epithelium regulates bacterial infection in mice.Mucosal immunology · 2012Article
- Bacterial chemotaxis modulates host cell apoptosis to establish a T-helper cell, type 17 (Th17)-dominant immune response in Helicobacter pylori infection.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- Helicobacter pylori and gastric cancer: factors that modulate disease risk.Clinical microbiology reviews · 2010Review
- Interplay between Helicobacter pylori and immune cells in immune pathogenesis of gastric inflammation and mucosal pathology.Cellular & molecular immunology · 2010Review
- Cytotoxic T cells in H. pylori-related gastric autoimmunity and gastric lymphoma.Journal of biomedicine & biotechnology · 2010Review
- Akt and SHIP modulate Francisella escape from the phagosome and induction of the Fas-mediated death pathway.PloS one · 2009Article
- Upregulation of CCL20 and recruitment of CCR6+ gastric infiltrating lymphocytes in Helicobacter pylori gastritis.Infection and immunity · 2007Article
- Distinct patterns of mucosal apoptosis in H pylori-associated gastric ulcer are associated with altered FasL and perforin cytotoxic pathways.World journal of gastroenterology · 2006Article
- Immune response to H. pylori.World journal of gastroenterology · 2006Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 4 countries.
Funding
Abstract
Helicobacter pylori causes a common chronic infection of humans that leads to epithelial cell damage. Studies have shown that apoptosis of the gastric epithelium is increased during infection and this response is associated with an expansion of gastric T-helper type 1 (Th1) cells. We report that gastric T cells contribute to apoptosis of the epithelium by a Fas/Fas ligand (FasL) interaction. Fas receptor expression was detected on freshly isolated gastric epithelial cells by flow cytometry and immunohistochemistry, and this level of expression was increased during infection with H. pylori. The expression of Fas receptor on three gastric epithelial cell lines was increased by H. pylori, either alone or in combination with gamma interferon or tumor necrosis factor alpha. The role of Fas in apoptosis of gastric epithelial cell lines was evidenced by DNA fragmentation after cross-linking of Fas with specific antibodies. FasL expression was detected by immunohistochemistry on mononuclear cells in gastric biopsy specimens of infected but not uninfected subjects. Gastric T-cell lines were also shown to express FasL, as evidenced by reverse transcription-PCR and killing of target cells expressing Fas receptor. Moreover, these T-cell lines were capable of killing cultured gastric epithelial target cells and antibodies that block the interaction between Fas receptor and FasL inhibited this cytotoxic activity. These observations demonstrate that local Th1 cells may contribute to the pathogenesis of gastric disease during H. pylori infection by increasing the expression of Fas on gastric epithelial cells and inducing apoptosis through Fas/FasL interactions.
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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.