Evidence map›Paper›PMID 19917709›Full record

ArticleInfection and immunity2010

Helicobacter pylori stimulates dendritic cells to induce interleukin-17 expression from CD4+ T lymphocytes.

Wafa Khamri, Marjorie M Walker, Peter Clark, John C Atherton, Mark R Thursz, Kathleen B Bamford, Robert I Lechler, Giovanna Lombardi

Open access · greenAbstract read
In one paragraph

Article in Infection and immunity, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
7.4field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

50 citing papers in PubMed, 102 citations in OpenAlex.

  1. Trial
  2. Beyond the Stomach: Exploring the Role ofExpert reviews in molecular medicine · 2026
    Review
  3. Review
  4. UnravelingVaccines · 2025
    Review
  5. Article
  6. Effects ofFrontiers in cellular and infection microbiology · 2024
    Review
  7. Pivotal role ofFrontiers in medicine · 2024
    Review
  8. Article
  9. Immune Biology and Persistence of Helicobacter pylori in Gastric Diseases.Current topics in microbiology and immunology · 2023
    Article
  10. Innate Immunity Crosstalk withInternational journal of molecular sciences · 2022
    Review
  11. Article
  12. Infection and drug resistance · 2022
    Review
  13. Article
  14. Review
  15. Review
  16. Two Distinct Etiologies of Gastric Cancer: Infection and Autoimmunity.Frontiers in cell and developmental biology · 2021
    Review
  17. Article
  18. TLR2, TLR4 and TLR10 Shape the Cytokine and Chemokine Release ofInternational journal of molecular sciences · 2020
    Article
  19. Dual infective burden of Helicobacter pylori and intestinal parasites: Good or bad news for the host?Indian journal of gastroenterology : official journal of the Indian Society of Gastroenterology · 2020
    Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 4 institutions in 1 country.

Wafa KhamriImmunoregulation Laboratory, Department of Nephrology and Transplantation, 5th Floor Thomas Guy House, Guy's Hospital Campus, King's College London School of Medicine at Guy's, London SE1 9RT, United Kingdom. wafa.khamri@kcl.ac.uk
Marjorie M Walker
Peter Clark
John C Atherton
Mark R Thursz
Kathleen B Bamford
Robert I Lechler
Giovanna Lombardi
Imperial College London · GBGuy's Hospital · GBKing's College London · GBUniversity of Nottingham · GB

Funding

British Heart Foundation RG/08/005/25303
6 · The paper itself

Abstract

Helicobacter pylori is a human gastroduodenal pathogen that leads to active chronic inflammation characterized by T-cell responses biased toward a Th1 phenotype. It has been accepted that H. pylori infection induces a Th17 response. At mucosal sites, dendritic cells (DCs) have the capacity to induce effector T cells. Here, we evaluate the role of DCs in the H. pylori-induced interleukin-17 (IL-17) response. Immunohistochemistry and immunofluorescence were performed on human gastric mucosal biopsy samples and showed that myeloid DCs in H. pylori-infected patients colocalized with IL-23- and that IL-17-producing lymphocytes were present in H. pylori-infected antral biopsy samples. In parallel, human monocyte-derived DCs stimulated in vitro with live H. pylori cells produced significant levels of IL-23 in the absence of IL-12 release. The subsequent incubation of H. pylori-infected DCs with autologous CD4(+) T cells led to gamma interferon (IFN-gamma) and IL-17 expression. The inhibition of IL-1 and, to a lesser extent, IL-23 inhibited IL-17 production by T cells. Finally, isogenic H. pylori mutant strains not expressing major virulence factors were less effective in inducing IL-1 and IL-23 release by DCs and IL-17 release by T cells than parental strains. Altogether, we can conclude that DCs are potent inducers of IL-23/IL-17 expression following H. pylori stimulation. IL-1/IL-23 as well as H. pylori virulence factors seem to play an important role in mediating this response.

Indexed as

CD4-Positive T-LymphocytesCell SeparationDendritic CellsEnzyme-Linked Immunosorbent AssayFlow CytometryFluorescent Antibody TechniqueGastric MucosaHelicobacter InfectionsHelicobacter pyloriHumansImmunohistochemistryInterleukin-17Interleukin-23Lymphocyte ActivationMicroscopy, ConfocalReverse Transcriptase Polymerase Chain ReactionInterleukin-17Interleukin-23

Identifiers

PMID19917709
PMCPMC2812220
OpenAlexW2169007953

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.