Evidence map›Paper›PMID 22529299›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2012

Stem cell factor programs the mast cell activation phenotype.

Tomonobu Ito, Daniel Smrž, Mi-Yeon Jung, Geethani Bandara, Avanti Desai, Šárka Smržová, Hye Sun Kuehn, Michael A Beaven, Dean D Metcalfe, Alasdair M Gilfillan

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

60 citing papers in PubMed, 109 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. IL-33 induces histidine decarboxylase, especially in c-kitInflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023
    Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. KIT as a master regulator of the mast cell lineage.The Journal of allergy and clinical immunology · 2022
    Review
  17. Article
  18. Optimizing drug inhibition of IgE-mediated anaphylaxis in mice.The Journal of allergy and clinical immunology · 2022
    Article
  19. Review
  20. Review
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

10 authors at 2 institutions in 1 country.

Tomonobu ItoLaboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
Daniel Smrž
Mi-Yeon Jung
Geethani Bandara
Avanti Desai
Šárka Smržová
Hye Sun Kuehn
Michael A Beaven
Dean D Metcalfe
Alasdair M Gilfillan
National Institutes of Health · USNational Institute of Allergy and Infectious Diseases · 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
Critical signaling nodes regulating mast cell releasibility phenotypesZIAAI000967 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI METCALFE, DEAN D · 2009 to 2012
$1.4M
Intramural NIH HHS ZIA AI000965
6 · The paper itself

Abstract

Mast cells, activated by Ag via FcεRI, release an array of proinflammatory mediators that contribute to allergic disorders, such as asthma and anaphylaxis. The KIT ligand, stem cell factor (SCF), is critical for mast cell expansion, differentiation, and survival, and under acute conditions, it enhances mast cell activation. However, extended SCF exposure in vivo conversely protects against fatal Ag-mediated anaphylaxis. In investigating this dichotomy, we identified a novel mode of regulation of the mast cell activation phenotype through SCF-mediated programming. We found that mouse bone marrow-derived mast cells chronically exposed to SCF displayed a marked attenuation of FcεRI-mediated degranulation and cytokine production. The hyporesponsive phenotype was not a consequence of altered signals regulating calcium flux or protein kinase C, but of ineffective cytoskeletal reorganization with evidence implicating a downregulation of expression of the Src kinase Hck. Collectively, these findings demonstrate a major role for SCF in the homeostatic control of mast cell activation with potential relevance to mast cell-driven disease and the development of novel approaches for the treatment of allergic disorders.

Indexed as

AnimalsBone Marrow CellsCell DegranulationCell ProliferationCells, CulturedCoculture TechniquesHomeostasisHypersensitivityImmunophenotypingMast CellsMiceMice, Inbred C57BLNIH 3T3 CellsStem Cell FactorStem Cell Factor

Identifiers

PMID22529299
PMCPMC3358494
OpenAlexW2167204769

What OpenQuestion 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 OpenQuestion graph.