ArticleJournal of innate immunity2015
Helicobacter pylori inhibits dendritic cell maturation via interleukin-10-mediated activation of the signal transducer and activator of transcription 3 pathway.
Article in Journal of innate immunity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed.
- Helicobacter pylori eradication in the face of escalating anti-microbial resistance: Geographic heterogeneity and emerging treatment strategies.Indian journal of gastroenterology : official journal of the Indian Society of Gastroenterology · 2026Review
- A vicious cycle inducer in gastric pathogenesis: implication of Helicobacter pylori.Archives of microbiology · 2026Review
- Screening and functional validation of key genes inFrontiers in immunology · 2026Article
- The effects of postbiotics and glycyrrhetinic acid on immune response and inflammation-related genes during H. pylori eradication therapy.BMC microbiology · 2025Article
- The gut microbiota in cancer immunity and immunotherapy.Cellular & molecular immunology · 2025Review
- Recent advances in the mechanisms of PD-L1 expression in gastric cancer: a review.Biological research · 2025Review
- CD4European journal of medical research · 2024Article
- Pharmacogenomic and epigenomic approaches to untangle the enigma of IL-10 blockade in oncology.Expert reviews in molecular medicine · 2024Review
- Notch Signaling Regulates the Function and Phenotype of Dendritic Cells inMicroorganisms · 2023Article
- A review of signal pathway induced by virulent protein CagA ofFrontiers in cellular and infection microbiology · 2023Review
- Helicobacter Pylori and Gastric Cancer Progression.Current microbiology · 2022Review
- The Structural Characterization and Immunomodulatory Activity of Polysaccharides fromNutrients · 2022Article
- Article
- Emerging Role ofFrontiers in oncology · 2022Review
- Targeting myeloid villains in the treatment with immune checkpoint inhibitors in gastrointestinal cancer.Frontiers in immunology · 2022Review
- IL-10Frontiers in immunology · 2021Article
- Helicobacter-stimulated IL-10-producing B cells suppress differentiation of lipopolysaccharide/Helicobacter felis-activated stimulatory dendritic cells.Turkish journal of biology = Turk biyoloji dergisi · 2021Article
- Dietary intake of walnut preventedJournal of clinical biochemistry and nutrition · 2021Article
- Walnut polyphenol extracts inhibitJournal of clinical biochemistry and nutrition · 2020Article
- Interleukin-21 (IL-21) Downregulates Dendritic Cell Cytokine Responses to Helicobacter pylori and Modulates T Lymphocyte IL-17A Expression in Peyer's Patches during Infection.Infection and immunity · 2019Article
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
Helicobacter pylori infects the human gastric mucosa causing a chronic infection that is the primary risk factor for gastric cancer development. Recent studies demonstrate that H. pylori promotes tolerogenic dendritic cell (DC) development indicating that this bacterium evades the host immune response. However, the signaling pathways involved in modulating DC activation during infection remain unclear. Here, we report that H. pylori infection activated the signal transducer and activator of transcription 3 (STAT3) pathway in murine bone marrow-derived DCs (BMDCs) and splenic DCs isolated ex vivo. Isogenic cagA-, cagE-, vacA- and urease-mutants exhibited levels of phosphoSTAT3 that were comparable to in the wild-type (WT) parent strain. H. pylori-infected BMDCs produced increased immunosuppressive IL-10, which activated STAT3 in an autocrine/paracrine fashion. Neutralization of IL-10 prevented H. pylori-mediated STAT3 activation in both BMDCs and splenic DCs. In addition, anti-IL-10 treatment of infected H. pylori-BMDCs was associated with increased CD86 and MHC II expression and enhanced proinflammatory IL-1β cytokine secretion. Finally, increased CD86 and MHC II expression was detected in H. pylori-infected STAT3 knockout DCs when compared to WT controls. Together, these results demonstrate that H. pylori infection induces IL-10 secretion in DCs, which activates STAT3, thereby modulating DC maturation and reducing IL-1β secretion. These findings identify a host molecular mechanism by which H. pylori can manipulate the innate immune response to potentially favor chronic infection and promote carcinogenesis.
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