Evidence map›Paper›PMID 23757302›Full record

ArticleMucosal immunology2014

Basophils control T-cell responses and limit disease activity in experimental murine colitis.

M Rodriguez Gomez, Y Talke, C Hofmann, I Ketelsen, F Hermann, B Reich, N Goebel, K Schmidbauer, N Dunger, H Brühl and 3 more

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Mucosal immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

31 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. IL-3: key orchestrator of inflammation.Frontiers in immunology · 2024
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. Review
  14. Article
  15. Review
  16. Frontiers in immunology · 2018
    Article
  17. Article
  18. Article
  19. Article
  20. Basophil-derived IL-6 regulates TScientific reports · 2017
    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

13 authors at 1 institution in 1 country.

M Rodriguez GomezDepartment of Internal Medicine II, University Hospital Regensburg, Regensburg, Germany.
Y TalkeDepartment of Internal Medicine II, University Hospital Regensburg, Regensburg, Germany.
C HofmannDepartment of Internal Medicine I, University Hospital Regensburg, Regensburg, Germany.
I KetelsenDepartment of Internal Medicine II, University Hospital Regensburg, Regensburg, Germany.
F HermannDepartment of Internal Medicine II, University Hospital Regensburg, Regensburg, Germany.
B ReichDepartment of Internal Medicine II, University Hospital Regensburg, Regensburg, Germany.
N GoebelDepartment of Internal Medicine II, University Hospital Regensburg, Regensburg, Germany.
K SchmidbauerDepartment of Internal Medicine II, University Hospital Regensburg, Regensburg, Germany.
N DungerDepartment of Internal Medicine I, University Hospital Regensburg, Regensburg, Germany.
H BrühlDepartment of Internal Medicine I, University Hospital Regensburg, Regensburg, Germany.
K RennerDepartment of Internal Medicine II, University Hospital Regensburg, Regensburg, Germany.
S-N SyedDepartment of Internal Medicine II, University Hospital Regensburg, Regensburg, Germany.
M MackDepartment of Internal Medicine II, University Hospital Regensburg, Regensburg, Germany.
University Hospital Regensburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Basophils have been recognized as important inducers of T helper type 2 (Th2) responses. Using the colitis model of adoptive transfer of CD4(+) CD62L(+) T cells into lymphopenic hosts, we have analyzed how basophils regulate T-cell responses and modulate disease activity. Transferred T cells rapidly proliferate, produce large amounts of interleukin (IL)-3, and expand the number of basophils in an IL-3-dependent manner. Depletion of basophils with two different antibodies substantially upregulated Th1 cytokines in transferred T cells at day 8. Increased Th1 cytokine expression persisted until the end of the experiment when basophil-depleted mice showed exacerbation of colitis with more severe loss of weight, histological damage, colonic leukocyte infiltration, and expression of pro-inflammatory cytokines. In vitro, we show that basophil-derived IL-4 and IL-6 downregulates expression of interferon-γ, IL-2, and tumor necrosis factor in T cells. These data show a beneficial role of basophils in a T-cell driven model of autoimmunity.

Indexed as

Adoptive TransferAnimalsBasophilsColitisCytokinesDisease Models, AnimalFemaleLymphopeniaMaleMiceMice, KnockoutPhenotypeTh1 CellsT-LymphocytesCytokines

Identifiers

PMID23757302
OpenAlexW2049065673

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.