Evidence map›Paper›PMID 25779634›Full record

ArticleThe Journal of experimental medicine2015

IgE-activated basophils regulate eosinophil tissue entry by modulating endothelial function.

Laurence E Cheng, Brandon M Sullivan, Lizett E Retana, Christopher D C Allen, Hong-Erh Liang, Richard M Locksley

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 1 pooled it
6.2field-weighted citation impact, top 3% 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

42 citing papers in PubMed, 1 synthesis or guideline pooled it, 81 citations in OpenAlex.

  1. Eosinophils and eosinophil-associated diseases: An update.The Journal of allergy and clinical immunology · 2018
    Pooled it
  2. Gastrointestinal Eosinophil Responses in a Longitudinal, Randomized Trial of Peanut Oral Immunotherapy.Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association · 2021
    Trial
  3. Article
  4. Review
  5. Review
  6. Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Review
  19. Article
  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

6 authors at 4 institutions in 2 countries.

Laurence E ChengDepartment of Pediatrics, Department of Medicine, Department of Anatomy, Sandler Asthma Basic Research Center, Cardiovascular Research Institute, Department of Microbiology and Immunology, and Howard Hughes Medical Institute, University of California, San Francisco, San Francisco, CA 94143 Department of Pediatrics, Department of Medicine, Department of Anatomy, Sandler Asthma Basic Research Center, Cardiovascular Research Institute, Department of Microbiology and Immunology, and Howard Hughes Medical Institute, University of California, San Francisco, San Francisco, CA 94143.
Brandon M SullivanDepartment of Pediatrics, Department of Medicine, Department of Anatomy, Sandler Asthma Basic Research Center, Cardiovascular Research Institute, Department of Microbiology and Immunology, and Howard Hughes Medical Institute, University of California, San Francisco, San Francisco, CA 94143.
Lizett E RetanaDepartment of Pediatrics, Department of Medicine, Department of Anatomy, Sandler Asthma Basic Research Center, Cardiovascular Research Institute, Department of Microbiology and Immunology, and Howard Hughes Medical Institute, University of California, San Francisco, San Francisco, CA 94143.
Christopher D C AllenDepartment of Pediatrics, Department of Medicine, Department of Anatomy, Sandler Asthma Basic Research Center, Cardiovascular Research Institute, Department of Microbiology and Immunology, and Howard Hughes Medical Institute, University of California, San Francisco, San Francisco, CA 94143 Department of Pediatrics, Department of Medicine, Department of Anatomy, Sandler Asthma Basic Research Center, Cardiovascular Research Institute, Department of Microbiology and Immunology, and Howard Hughes Medical Institute, University of California, San Francisco, San Francisco, CA 94143 Department of Pediatrics, Department of Medicine, Department of Anatomy, Sandler Asthma Basic Research Center, Cardiovascular Research Institute, Department of Microbiology and Immunology, and Howard Hughes Medical Institute, University of California, San Francisco, San Francisco, CA 94143.
Hong-Erh LiangDepartment of Pediatrics, Department of Medicine, Department of Anatomy, Sandler Asthma Basic Research Center, Cardiovascular Research Institute, Department of Microbiology and Immunology, and Howard Hughes Medical Institute, University of California, San Francisco, San Francisco, CA 94143.
Richard M LocksleyDepartment of Pediatrics, Department of Medicine, Department of Anatomy, Sandler Asthma Basic Research Center, Cardiovascular Research Institute, Department of Microbiology and Immunology, and Howard Hughes Medical Institute, University of California, San Francisco, San Francisco, CA 94143 Department of Pediatrics, Department of Medicine, Department of Anatomy, Sandler Asthma Basic Research Center, Cardiovascular Research Institute, Department of Microbiology and Immunology, and Howard Hughes Medical Institute, University of California, San Francisco, San Francisco, CA 94143 Department of Pediatrics, Department of Medicine, Department of Anatomy, Sandler Asthma Basic Research Center, Cardiovascular Research Institute, Department of Microbiology and Immunology, and Howard Hughes Medical Institute, University of California, San Francisco, San Francisco, CA 94143 Department of Pediatrics, Department of Medicine, Department of Anatomy, Sandler Asthma Basic Research Center, Cardiovascular Research Institute, Department of Microbiology and Immunology, and Howard Hughes Medical Institute, University of California, San Francisco, San Francisco, CA 94143 locksley@medicine.ucsf.edu.
Pediatrics and Genetics · USCardiovascular Institute Hospital · JPHoward Hughes Medical Institute · USUniversity of California, San Francisco · US

Funding

Role of miRNAs in Th2-Driven inflammation in AsthmaP01HL107202 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI FAHY, JOHN V · 2012 to 2023
$23.3M
Initiation of allergic immunity by parasitesR01AI030663 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI LOCKSLEY, RICHARD M · 1991 to 2016
$5.7M
Parasite immunity orchestrated by type 2 immune cellsR01AI026918 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI LOCKSLEY, RICHARD M · 1988 to 2022
$3.8M
Parasite Immunity Orchestrated by Th2 CellsR37AI026918 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI LOCKSLEY, RICHARD M · 2006 to 2015
$3.8M
Analysis of basophil function in secondary immune responsesR01AI103146 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI ALLEN, CHRISTOPHER DAVID CABALLERO · 2013 to 2017
$1.9M
Surveillance of Serum Contents by Mast Cells and Regulation of Allergic ImmunityK08AI095319 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI CHENG, LAURENCE E · 2011 to 2014
$510k
Howard Hughes Medical InstituteNHLBI NIH HHS P01 HL107202NIAID NIH HHS AI026918NIAID NIH HHS AI030663NIAID NIH HHS AI095319NIAID NIH HHS AI119944NIAID NIH HHS K08 AI095319NIAID NIH HHS R01 AI026918NIAID NIH HHS R01 AI030663NIAID NIH HHS R01 AI103146NIAID NIH HHS R37 AI026918
6 · The paper itself

Abstract

Vertebrate immunity has evolved a modular architecture in response to perturbations. Allergic inflammation represents such a module, with signature features of antigen-specific IgE and tissue eosinophilia, although the cellular and molecular circuitry coupling these responses remains unclear. Here, we use genetic and imaging approaches in models of IgE-dependent eosinophilic dermatitis to demonstrate a requisite role for basophils. After antigenic inflammation, basophils initiate transmigration like other granulocytes but, upon activation via their high-affinity IgE receptor, alter their migratory kinetics to persist at the endothelium. Prolonged basophil-endothelial interactions, in part dependent on activation of focal adhesion kinases, promote delivery of basophil-derived IL-4 to the endothelium and subsequent induction of endothelial vascular cell adhesion molecule-1 (VCAM-1), which is required for eosinophil accumulation. Thus, basophils are gatekeepers that link adaptive immunity with innate effector programs by altering access to tissue sites by activation-induced interactions with the endothelium.

Indexed as

AnimalsBasophilsCell CommunicationDermatitisEndothelial CellsEosinophilsImmunity, InnateImmunoglobulin EInterleukin-4MiceMice, KnockoutTransendothelial and Transepithelial MigrationVascular Cell Adhesion Molecule-1Immunoglobulin EInterleukin-4Vascular Cell Adhesion Molecule-1

Identifiers

PMID25779634
PMCPMC4387286
OpenAlexW2164167723

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.