ArticleInfection and immunity2007
Chronic exposure to Helicobacter pylori impairs dendritic cell function and inhibits Th1 development.
Article in Infection and immunity, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 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.
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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
47 citing papers in PubMed, 96 citations in OpenAlex.
- Evaluation of the potential inhibitory activity of a combination of L. acidophilus, L. rhamnosus and L. sporogenes on Helicobacter pylori: A randomized double-blind placebo-controlled clinical trial.Chinese journal of integrative medicine · 2017Trial
- Autophagy: Mechanisms and therapeutic perspectives in intestinal metaplasia (Review).Molecular medicine reports · 2026Review
- Recent advances in the mechanisms of PD-L1 expression in gastric cancer: a review.Biological research · 2025Review
- The influence ofFrontiers in immunology · 2025Article
- Innate Immunity Crosstalk withInternational journal of molecular sciences · 2022Review
- Review
- Article
- Immunological markers andBiomedical reports · 2020Article
- TLR4 signaling improves PD-1 blockade therapy during chronic viral infection.PLoS pathogens · 2019Article
- Decreased IL-17RB expression impairs CD11bCell death & disease · 2019Article
- Review
- The Mechanisms UnderlyingTanaffos · 2017Review
- Schlafen 4-expressing myeloid-derived suppressor cells are induced during murine gastric metaplasia.The Journal of clinical investigation · 2016Article
- Loss of gastrokine-2 drives premalignant gastric inflammation and tumor progression.The Journal of clinical investigation · 2016Article
- Morphological and Cellular Features of Innate Immune Reaction in Helicobacter pylori Gastritis: A Brief Review.International journal of molecular sciences · 2016Review
- Systems-wide analyses of mucosal immune responses to Helicobacter pylori at the interface between pathogenicity and symbiosis.Gut microbes · 2016Review
- Suppression of cell division-associated genes by Helicobacter pylori attenuates proliferation of RAW264.7 monocytic macrophage cells.Scientific reports · 2015Article
- Lactic acid bacteria strains exert immunostimulatory effect on H. pylori-induced dendritic cells.Journal of immunology research · 2015Article
- Article
- Immune evasion strategies used by Helicobacter pylori.World journal of gastroenterology · 2014Review
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Helicobacter pylori causes chronic gastric infection that affects the majority of the world's population. Despite generating an inflammatory response, the immune system usually fails to clear the infection. Since dendritic cells (DCs) play a pivotal role in shaping the immune response, we investigated the effects of H. pylori on DC function. We have demonstrated that H. pylori increased the expression of activation markers on DCs while upregulating the inhibitory B7 family molecule, PD-L1. Functionally, H. pylori-treated DCs resulted in the production of interleukin-10 (IL-10) and IL-23 but not of alpha interferon (IFN-alpha). While very little or no IL-12 was produced to H. pylori alone, simultaneous ligation of CD40 on DCs induced IL-12 release. We also demonstrated that DCs treated with H. pylori-induced IFN-gamma production by allogeneic naive T cells. However, stimulation of DCs with H. pylori for an extended period of time impaired their ability to produce cytokines after CD40 ligation and limited their ability to promote IFN-gamma release, suggesting that the DCs had become exhausted by the prolonged stimulation. The effect of chronic infection with H. pylori on DC function was further investigated by focusing on DC development. Demonstrating that monocytes differentiated into DCs in the presence of H. pylori exhibited an exhausted phenotype with an impaired ability to produce IL-12 and a downregulation of CD1a. Our results raise the possibility that in chronic H. pylori infection DCs become exhausted after prolonged antigen exposure leading to suboptimal Th1 development. This effect may contribute to persistence of H. pylori infection.
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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.