ArticlePloS one2015
Helicobacter pylori cag pathogenicity island's role in B7-H1 induction and immune evasion.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 39 citations in OpenAlex.
- Myeloid-derived suppressor cells modulation in the context of tumor microenvironment for gastric cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025Review
- Research progress on the impact and mechanisms of helicobacter pylori infection on the efficacy of immunotherapy for gastric cancer.Frontiers in oncology · 2025Review
- Effects and mechanisms ofFrontiers in immunology · 2024Review
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- Signaling pathways and therapeutic interventions in gastric cancer.Signal transduction and targeted therapy · 2022Review
- Constitutive programmed death ligand 1 expression protects gastric G-cells from Helicobacter pylori-induced inflammation.Helicobacter · 2022Article
- Review
- Article
- Effects ofFrontiers in immunology · 2022Review
- A Multi-Omics Study on the Effect of Helicobacter Pylori-Related Genes in the Tumor Immunity on Stomach Adenocarcinoma.Frontiers in cellular and infection microbiology · 2022Article
- Role of PD-L1 in Gut Mucosa Tolerance and Chronic Inflammation.International journal of molecular sciences · 2020Review
- Current status of immune checkpoint inhibitors for gastric cancer.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2020Review
- Th17 Cells in Helicobacter pylori Infection: a Dichotomy of Help and Harm.Infection and immunity · 2019Review
- Novel Insights of Lymphomagenesis ofCancers · 2019Review
- Helicobacter pylori Deregulates T and B Cell Signaling to Trigger Immune Evasion.Current topics in microbiology and immunology · 2019Review
- Article
- Gastric Cancer in the Era of Immune Checkpoint Blockade.Journal of oncology · 2019Review
- Prevention of Gastric Cancer: Eradication of Helicobacter Pylori and Beyond.International journal of molecular sciences · 2017Review
- Helicobacter Pylori Promote B7-H1 Expression by Suppressing miR-152 and miR-200b in Gastric Cancer Cells.PloS one · 2017Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
During Helicobacter pylori (H. pylori) infection CD4+ T cells in the gastric lamina propria are hyporesponsive and polarized by Th1/Th17 cell responses controlled by Treg cells. We have previously shown that H. pylori upregulates B7-H1 expression on GEC, which, in turn, suppress T cell proliferation, effector function, and induce Treg cells in vitro. In this study, we investigated the underlying mechanisms and the functional relevance of B7-H1 induction by H. pylori infection to chronic infection. Using H. pylori wild type (WT), cag pathogenicity island (cag PAI-) and cagA- isogenic mutant strains we demonstrated that H. pylori requires its type 4 secretion system (T4SS) as well as its effector protein CagA and peptidoglycan (PG) fragments for B7-H1 upregulation on GEC. Our study also showed that H. pylori uses the p38 MAPK pathway to upregulate B7-H1 expression in GEC. In vivo confirmation was obtained when infection of C57BL/6 mice with H. pylori PMSS1 strain, which has a functional T4SS delivery system, but not with H. pylori SS1 strain lacking a functional T4SS, led to a strong upregulation of B7-H1 expression in the gastric mucosa, increased bacterial load, induction of Treg cells in the stomach, increased IL-10 in the serum. Interestingly, B7-H1-/- mice showed less Treg cells and reduced bacterial loads after infection. These studies demonstrate how H. pylori T4SS components activate the p38 MAPK pathway, upregulate B7-H1 expression by GEC, and cause Treg cell induction; thus, contribute to establishing a persistent infection characteristic of H. pylori.
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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.