Evidence map›Paper›PMID 24412367›Full record

ArticleCell reports2014

Critical role for mast cell Stat5 activity in skin inflammation.

Tomoaki Ando, Wenbin Xiao, Peisong Gao, Siavash Namiranian, Kenji Matsumoto, Yoshiaki Tomimori, Hong Hong, Hirotaka Yamashita, Miho Kimura, Jun-Ichi Kashiwakura and 9 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell reports, 2014. 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
4.3field-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, 89 citations in OpenAlex.

  1. Phospholipases: Where Do We Stand?Methods in molecular biology (Clifton, N.J.) · 2027
    Review
  2. Article
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  4. Article
  5. Review
  6. Article
  7. Research Progress in Skin Aging and Immunity.International journal of molecular sciences · 2024
    Review
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  9. Article
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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

19 authors at 9 institutions in 3 countries.

Tomoaki AndoDivision of Cell Biology, La Jolla Institute for Allergy and Immunology, La Jolla, CA 92037, USA.
Wenbin XiaoDivision of Cell Biology, La Jolla Institute for Allergy and Immunology, La Jolla, CA 92037, USA.
Peisong GaoDivision of Allergy and Clinical Immunology, Johns Hopkins University, Baltimore, MD 21224, USA.
Siavash NamiranianDepartment of Bioengineering, University of California San Diego, La Jolla, CA 92093, USA.
Kenji MatsumotoDepartment of Allergy and Immunology, National Research Institute for Child Health and Development, Tokyo 157-8535, Japan.
Yoshiaki TomimoriDivision of Cell Biology, La Jolla Institute for Allergy and Immunology, La Jolla, CA 92037, USA.
Hong HongDivision of Cell Biology, La Jolla Institute for Allergy and Immunology, La Jolla, CA 92037, USA.
Hirotaka YamashitaDivision of Cell Biology, La Jolla Institute for Allergy and Immunology, La Jolla, CA 92037, USA.
Miho KimuraDivision of Cell Biology, La Jolla Institute for Allergy and Immunology, La Jolla, CA 92037, USA.
Jun-Ichi KashiwakuraLaboratory for Allergic Disease, RIKEN Center for Integrative Medical Sciences (IMS-RCAI), Yokohama 230-0045, Japan.
Tissa R HataDivision of Dermatology, Department of Medicine, University of California San Diego, La Jolla, CA 92037, USA.
Kenji IzuharaDivision of Medical Biochemistry, Department of Biomolecular Sciences and Department of Laboratory Medicine, Saga Medical School, Saga 849-85-01, Japan.
Michael F GurishDepartment of Medicine, Brigham and Women's Hospital, Boston, MA 02115, USA.
Axel RoersInstitute for Immunology, University of Technology Dresden, Medical Faculty Carl-Gustav Carus, 01307 Dresden, Germany.
Nicholas M RafaelsDivision of Allergy and Clinical Immunology, Johns Hopkins University, Baltimore, MD 21224, USA.
Kathleen C BarnesDivision of Allergy and Clinical Immunology, Johns Hopkins University, Baltimore, MD 21224, USA.
Colin JamoraDepartment of Bioengineering, University of California San Diego, La Jolla, CA 92093, USA.
Yuko KawakamiDivision of Cell Biology, La Jolla Institute for Allergy and Immunology, La Jolla, CA 92037, USA.
Toshiaki KawakamiDivision of Cell Biology, La Jolla Institute for Allergy and Immunology, La Jolla, CA 92037, USA; Laboratory for Allergic Disease, RIKEN Center for Integrative Medical Sciences (IMS-RCAI), Yokohama 230-0045, Japan. Electronic address: toshi@lji.org.
La Jolla Institute for Immunology · USUniversity of California, San Diego · USJohns Hopkins Medicine · USBrigham and Women's Hospital · USJohns Hopkins University · USNational Center For Child Health and Development · JPRIKEN Center for Integrative Medical Sciences · JPSaga Medical School Hospital · JPUniversity Hospital Carl Gustav Carus · DE

Funding

IgE Regulation of Mast Cell Growth and SurvivalR01AI050209 · NIAID · LA JOLLA INSTITUTE FOR IMMUNOLOGY · PI KAWAKAMI, TOSHIAKI · 2002 to 2006
$2.3M
Mast cell Stat5-regulatory pathway in atopic dermatitisR01AR064418 · NIAMS · LA JOLLA INSTITUTE FOR IMMUNOLOGY · PI KAWAKAMI, TOSHIAKI · 2014 to 2018
$1.9M
NIAID NIH HHS N01 AI040030NIAID NIH HHS R01 AI050209NIAMS NIH HHS R01 AR064418
6 · The paper itself

Abstract

Atopic dermatitis (AD) is a chronic inflammatory skin disease. Here, we show that phospholipase C-β3 (PLC-β3)-deficient mice spontaneously develop AD-like skin lesions and more severe allergen-induced dermatitis than wild-type mice. Mast cells were required for both AD models and remarkably increased in the skin of Plcb3(-/-) mice because of the increased Stat5 and reduced SHP-1 activities. Mast cell-specific deletion of Stat5 gene ameliorated allergen-induced dermatitis, whereas that of Shp1 gene encoding Stat5-inactivating SHP-1 exacerbated it. PLC-β3 regulates the expression of periostin in fibroblasts and TSLP in keratinocytes, two proteins critically involved in AD pathogenesis. Furthermore, polymorphisms in PLCB3, SHP1, STAT5A, and STAT5B genes were associated with human AD. Mast cell expression of PLC-β3 was inversely correlated with that of phospho-STAT5, and increased mast cells with high levels of phospho-STAT5 were found in lesional skin of some AD patients. Therefore, STAT5 regulatory mechanisms in mast cells are important for AD pathogenesis.

Indexed as

AnimalsDermatitis, AtopicGene DeletionHumansMast CellsMiceMice, Inbred C57BLPhospholipase C betaPolymorphism, Single NucleotideProtein Tyrosine Phosphatase, Non-Receptor Type 6SkinSTAT5 Transcription FactorPhospholipase C betaPlcb3 protein, mouseProtein Tyrosine Phosphatase, Non-Receptor Type 6STAT5 Transcription Factor

Identifiers

PMID24412367
PMCPMC4329986
OpenAlexW2049255950

What OpenQuestion holds

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LicenceCC BY-NC
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Registered trials

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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.