ArticleClinical and experimental immunology2011
Stimulation of dendritic cells with Helicobacter pylori vacuolating cytotoxin negatively regulates their maturation via the restoration of E2F1.
Article in Clinical and experimental immunology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 48 citations in OpenAlex.
- Helicobacter pylori is associated with less tumor-infiltrating lymphocytes and a poor prognosis in gastric cancer.BMC gastroenterology · 2025Article
- Single-cell RNA sequencing dissects the immunosuppressive signatures in Helicobacter pylori-infected human gastric ecosystem.Nature communications · 2025Article
- Microbiome influence in gastric cancer progression and therapeutic strategies.Frontiers in medicine · 2025Review
- Immune Biology and Persistence of Helicobacter pylori in Gastric Diseases.Current topics in microbiology and immunology · 2023Article
- Review
- The Roles of IL-17, IL-21, and IL-23 in theToxins · 2021Review
- Fighting Persistence: How Chronic Infections with Mycobacterium tuberculosis Evade T Cell-Mediated Clearance and New Strategies To Defeat Them.Infection and immunity · 2020Review
- Store-operated CaScientific reports · 2017Article
- Host pathogen interactions inWorld journal of gastroenterology · 2017Review
- Article
- Crude Preparations of Helicobacter pylori Outer Membrane Vesicles Induce Upregulation of Heme Oxygenase-1 via Activating Akt-Nrf2 and mTOR-IκB Kinase-NF-κB Pathways in Dendritic Cells.Infection and immunity · 2016Article
- Review
- Review
- Helicobacter pylori outer membrane vesicle proteins induce human eosinophil degranulation via a β2 Integrin CD11/CD18- and ICAM-1-dependent mechanism.Mediators of inflammation · 2015Article
- Immune evasion strategies used by Helicobacter pylori.World journal of gastroenterology · 2014Review
- Life in the human stomach: persistence strategies of the bacterial pathogen Helicobacter pylori.Nature reviews. Microbiology · 2013Review
- Helicobacter pylori γ-glutamyl transpeptidase and vacuolating cytotoxin promote gastric persistence and immune tolerance.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Helicobacter pylori induces in-vivo expansion of human regulatory T cells through stimulating interleukin-1β production by dendritic cells.Clinical and experimental immunology · 2012Article
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- Review
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Authors and funding
7 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Helicobacter pylori induces an infiltration of dendritic cells (DCs) into the infected gastric mucosa. Although DCs play an important role in the regulation of inflammation, the effects of H. pylori vacuolating cytotoxin (VacA) on DC maturation process have not yet been elucidated. The role of VacA in DC maturation following co-exposure to Escherichia coli lipopolysaccharide (LPS) was investigated. The treatment of immature DCs with LPS up-regulated the expression of surface molecules [e.g. CD40, CD80, CD86 and major histocompatibility complex (MHC) class II], as well as the production of cytokines [e.g. interleukin (IL)-1β, IL-12p70 and tumour necrosis gactor (TNF)-α] compared with those of unstimulated controls. Co-stimulation with H. pylori VacA significantly reduced the up-regulated DC maturation markers induced by LPS. In addition, VacA sustained the immature state of DCs with high endocytosis and low migratory capacity. The LPS-induced down-regulation of E2F1 expression in DCs was recovered by co-stimulation with VacA. Moreover, suppression of E2F1 by small interfering RNA resulted in a significant recovery of the inhibited DC maturation by VacA. In contrast, VacA did not affect nuclear factor (NF)-κB responses to LPS and the NF-κB signal was not associated with VacA-induced inhibition of DC maturation. These results suggest that the exposure of DCs to H. pylori VacA negatively regulates DC maturation via the restoration of E2F1. The immunomodulatory action of VacA on DCs may contribute to the ability of VacA-producing H. pylori to establish a persistent infection in the gastric mucosa.
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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.