Evidence map›Paper›PMID 12780684›Full record

ArticleClinical and experimental immunology2003

Absence of CD4+CD25+ regulatory T cells is associated with a loss of regulation leading to increased pathology in Helicobacter pylori-infected mice.

S Raghavan, M Fredriksson, A-M Svennerholm, J Holmgren, E Suri-Payer

Open access · greenAbstract read
In one paragraph

Article in Clinical and experimental immunology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed
16.2field-weighted citation impact, top 1% 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

65 citing papers in PubMed, 171 citations in OpenAlex.

  1. Developing a potent vaccine againstExpert reviews in molecular medicine · 2024
    Review
  2. Strategies ofFrontiers in cellular and infection microbiology · 2024
    Review
  3. Article
  4. Medical research archives · 2022
    Article
  5. Genetics of Host Protection againstInternational journal of molecular sciences · 2021
    Review
  6. T Cell Cytokines Impact Epithelial Cell Responses duringJournal of immunology (Baltimore, Md. : 1950) · 2020
    Review
  7. Review
  8. Immune Response to MucosalFrontiers in immunology · 2019
    Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Immune responses to Helicobacter pylori infection.World journal of gastroenterology · 2014
    Review
  17. Article
  18. Article
  19. Article
  20. Article

5 more citing papers are in PubMed but not listed here.

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

5 authors at 1 institution in 1 country.

S RaghavanDepartment of Medical Microbiology and Immunology, Göteborg University, Göteborg, Sweden. sukanya.raghavan@microbio.gu.se
M Fredriksson
A-M Svennerholm
J Holmgren
E Suri-Payer
University of Gothenburg · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Helicobacter pylori induces symptomatic chronic gastritis in a subpopulation of infected individuals. The mechanism(s) determining the development and severity of pathology leading to symptoms are not fully understood. In a mouse model of H. pylori infection we analysed the influence of immunoregulatory CD4+CD25+ T cells on H. pylori colonization and gastritis. Athymic C57BL/6 nu/nu mice were reconstituted with (a) lymph node (LN) cells (b) LN cells depleted of CD25+ T cells (CD25(-) LN) or (c) not reconstituted at all. Mice were then infected orally with 3 x 10(8)H. pylori SS1 bacteria. At 2 and 6 weeks after the inoculation there was a significant (P < 0.001) reduction in H. pylori colonization in athymic mice transferred with CD25(-) LN cells compared to mice transferred with LN cells. Colonization was still reduced at 12 weeks after inoculation. Mice transferred with CD25(-) LN cells showed an earlier onset and increased severity of gastritis as compared to mice receiving LN cells. Splenic cells isolated from mice receiving CD25(-) LN cells produced the highest level of IFN-gamma on stimulation with H. pylori antigens in vitro, had a higher H. pylori-specific DTH response and increased infiltration of CD4+ T cells and macrophages in the gastric mucosa. Athymic mice not transferred with T cells had persistent high H. pylori colonization and displayed a normal gastric epithelium without inflammatory cells. In conclusion, CD4+CD25+ cells reduce immunopathology in H. pylori infection, possibly by reducing the activation of IFN-gamma producing CD4+ T cells, even at the expense of a higher H. pylori load in the gastric mucosa.

Indexed as

Helicobacter pyloriImmune ToleranceAdoptive TransferAnimalsCD4-Positive T-LymphocytesChronic DiseaseDisease Models, AnimalFemaleGastritisHelicobacter InfectionsImmunity, CellularLymph NodesLymphocyte ActivationMiceMice, Inbred C57BLMice, NudeReceptors, Interleukin-2

Identifiers

PMID12780684
PMCPMC1808721
OpenAlexW1981690711

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.