Evidence map›Paper›PMID 26256265›Full record

ArticleEuropean journal of immunology2015

Activated mast cells synthesize and release soluble ST2-a decoy receptor for IL-33.

Geethani Bandara, Michael A Beaven, Ana Olivera, Alasdair M Gilfillan, Dean D Metcalfe

Open access · hybridAbstract read
In one paragraph

Article in European journal of immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

49 citing papers in PubMed, 87 citations in OpenAlex.

  1. Review
  2. Constitutively high levels of endogenous soluble ST2 inhibit food allergic responses in mice.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Human Lung Mast Cells: Therapeutic Implications in Asthma.International journal of molecular sciences · 2022
    Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Review
  16. Sex and age differences in sST2 in cardiovascular disease.Frontiers in cardiovascular medicine · 2022
    Article
  17. Review
  18. Article
  19. 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

5 authors at 3 institutions in 1 country.

Geethani BandaraLaboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.
Michael A BeavenLaboratory of Molecular Immunology, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD, USA.
Ana OliveraLaboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.
Alasdair M GilfillanLaboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.
Dean D MetcalfeLaboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.
National Institute of Allergy and Infectious Diseases · USNational Heart Lung and Blood Institute · USNational Institutes of Health · US

Funding

Integrated Signaling Pathways for the Enhancement of Mast Cell ActivationZIAAI000965 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI METCALFE, DEAN D · 2009 to 2018
$5.3M
Molecular Biology Of Mast Cell Growth &DifferentiationZ01AI000513 · NIAID · NIAID EXTRAMURAL ACTIVITIES · PI METCALFE, DEAN D · 1988 to 2008
$2.0M
Intramural NIH HHS Z01 AI000513Intramural NIH HHS ZIA AI000965
6 · The paper itself

Abstract

IL-33 released from damaged cells plays a central role in allergic inflammation by acting through its membrane-bound receptor, ST2 receptor (ST2L). IL-33 activity can be neutralized by the soluble spliced variant of ST2 (sST2) that has been associated with allergic inflammation but its source is not well defined. We investigated whether mast cells (MCs) are a significant source of sST2 following activation through FcεRI or ST2. We find that antigen and IL-33 induce substantial production and release of sST2 from human and mouse MCs in culture and do so synergistically when added together or in combination with stem cell factor. Moreover, increases in circulating sST2 during anaphylaxis in mice were dependent on the presence of MCs. Human MCs activated via FcεRI failed to generate IL-33 and IL-33 produced by mouse bone marrow-derived MCs was retained within the cells. Therefore, FcεRI-mediated sST2 production is independent of MC-derived IL-33 acting in an autocrine manner. These results are consistent with the conclusion that both mouse and human MCs when activated are a significant inducible source of sST2 but not IL-33 and thus have the ability to modulate the biologic impact of IL-33 produced locally by other cell types during allergic inflammation.

Indexed as

AnimalsCells, CulturedFlow CytometryHumansImmunoblottingInflammationInterleukin-1 Receptor-Like 1 ProteinInterleukin-33Mast CellsMiceMice, Inbred C57BLReal-Time Polymerase Chain ReactionReceptors, Cell SurfaceReceptors, InterleukinSignal TransductionIL1RL1 protein, humanIl1rl1 protein, mouseInterleukin-1 Receptor-Like 1 ProteinInterleukin-33Receptors, Cell SurfaceReceptors, InterleukinAntigenHuman mast cellsIL-33sST2Stem cell factor

Identifiers

PMID26256265
PMCPMC4813659
OpenAlexW2145409418

What Socratic holds

Textmetadata
LicenceTDM
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 Socratic graph.