Evidence map›Paper›PMID 31631836›Full record

ArticleeLife2019

Neutrophils promote CXCR3-dependent itch in the development of atopic dermatitis.

Carolyn M Walsh, Rose Z Hill, Jamie Schwendinger-Schreck, Jacques Deguine, Emily C Brock, Natalie Kucirek, Ziad Rifi, Jessica Wei, Karsten Gronert, Rachel B Brem and 2 more

Open access · goldAbstract read
In one paragraph

Article in eLife, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers.

0numbers the graph read from it
0cells of the map it votes in
86citing papers in PubMed
12.0field-weighted citation impact, top 1% 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

86 citing papers in PubMed, 152 citations in OpenAlex.

  1. Trial
  2. Lesional pruritus in pyoderma gangrenosum: Present but not predominant.JID innovations : skin science from molecules to population health · 2026
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  4. Cannabidiol-DominantNutrients · 2026
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  8. Cross-Organ Neuroimmunology of Behavior.Annual review of immunology · 2026
    Review
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  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article

26 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 2 institutions in 1 country.

Carolyn M Walsh *Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, United States.
Rose Z Hill *Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, United States.ORCID https://orcid.org/0000-0001-9558-6400
Jamie Schwendinger-SchreckDepartment of Molecular and Cell Biology, University of California, Berkeley, Berkeley, United States.
Jacques DeguineDepartment of Molecular and Cell Biology, University of California, Berkeley, Berkeley, United States.
Emily C BrockDepartment of Molecular and Cell Biology, University of California, Berkeley, Berkeley, United States.
Natalie KucirekDepartment of Molecular and Cell Biology, University of California, Berkeley, Berkeley, United States.
Ziad RifiDepartment of Molecular and Cell Biology, University of California, Berkeley, Berkeley, United States.
Jessica WeiVision Science Program, School of Optometry, University of California, Berkeley, Berkeley, United States.ORCID https://orcid.org/0000-0002-7329-2812
Karsten GronertVision Science Program, School of Optometry, University of California, Berkeley, Berkeley, United States.
Rachel B BremDepartment of Plant and Microbial Biology, University of California, Berkeley, Berkeley, United States.
Gregory M BartonDepartment of Molecular and Cell Biology, University of California, Berkeley, Berkeley, United States.ORCID https://orcid.org/0000-0002-3793-0100
Diana M BautistaDepartment of Molecular and Cell Biology, University of California, Berkeley, Berkeley, United States.ORCID https://orcid.org/0000-0002-6809-8951
University of California, Berkeley · USBuck Institute for Research on Aging · US

Funding

The role of Listeria cyclic-di-AMP during infection and immunityP01AI063302 · NIAID · UNIVERSITY OF CALIFORNIA BERKELEY · PI PORTNOY, DANIEL A · 2004 to 2025
$45.5M
The cell biology of Toll-like receptor 9: a mechanism to prevent autoimmunityR01AI072429 · NIAID · UNIVERSITY OF CALIFORNIA BERKELEY · PI Gregory M Barton · 2008 to 2026
$7.6M
NEUROBIOLOGY OF CORTICAL SYSTEMST32NS007224 · NINDS · YALE UNIVERSITY · PI CARDIN, JESSICA A · 1985 to 2025
$4.6M
Molecular Determinants of TLR TraffickingR01AI105184 · NIAID · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI BARTON, GREGORY M, CHANDA, SUMIT K · 2014 to 2017
$2.7M
Innate immunity and Salmonella pathogenesisR01AI104914 · NIAID · UNIVERSITY OF CALIFORNIA BERKELEY · PI BARTON, GREGORY M · 2013 to 2017
$1.7M
Roles and functions of ion channels that mediate mammalian touch transduction.R01AR059385 · NIAMS · UNIVERSITY OF CALIFORNIA BERKELEY · PI BAUTISTA, DIANA MICHELE · 2011 to 2015
$1.7M
Regulatory Tissue Polymorphonuclear Leukocytes Determinants of Ocular Immune ResponsesR01EY026082 · NEI · UNIVERSITY OF CALIFORNIA BERKELEY · PI GRONERT, KARSTEN · 2016 to 2019
$1.5M
Pacific Biosciences PacBio RS Single Molecule Real Time SequencerS10OD018174 · OD · UNIVERSITY OF CALIFORNIA BERKELEY · PI ROKHSAR, DANIEL SOLEYMAN · 2014 to 2014
$600k
Genetic Mapping of Novel Molecular Players in ItchR56NS098097 · NINDS · UNIVERSITY OF CALIFORNIA BERKELEY · PI BAUTISTA, DIANA MICHELE, BREM, RACHEL BETH · 2017 to 2017
$425k
Human Frontier Science Program LT-000081/2013-LNational Institute of Allergy and Infectious Diseases AI063302National Institute of Allergy and Infectious Diseases AI072429National Institute of Allergy and Infectious Diseases AI104914National Institute of Allergy and Infectious Diseases AI105184NEI NIH HHS EY026082NEI NIH HHS R01 EY026082NIAID NIH HHS P01 AI063302NIAID NIH HHS R01 AI072429NIAID NIH HHS R01 AI104914NIAID NIH HHS R01 AI105184NIAMS NIH HHS AR059385NIAMS NIH HHS R01 AR059385NIH HHS S10 OD018174NINDS NIH HHS NS07224NINDS NIH HHS NS098097NINDS NIH HHS R56 NS098097NINDS NIH HHS T32 NS007224
6 · The paper itself

Abstract

Chronic itch remains a highly prevalent disorder with limited treatment options. Most chronic itch diseases are thought to be driven by both the nervous and immune systems, but the fundamental molecular and cellular interactions that trigger the development of itch and the acute-to-chronic itch transition remain unknown. Here, we show that skin-infiltrating neutrophils are key initiators of itch in atopic dermatitis, the most prevalent chronic itch disorder. Neutrophil depletion significantly attenuated itch-evoked scratching in a mouse model of atopic dermatitis. Neutrophils were also required for several key hallmarks of chronic itch, including skin hyperinnervation, enhanced expression of itch signaling molecules, and upregulation of inflammatory cytokines, activity-induced genes, and markers of neuropathic itch. Finally, we demonstrate that neutrophils are required for induction of CXCL10, a ligand of the CXCR3 receptor that promotes itch via activation of sensory neurons, and we find that that CXCR3 antagonism attenuates chronic itch.

Indexed as

AnimalsCalcitriolCell LineChemokine CXCL10CytokinesDermatitis, AtopicDisease Models, AnimalGene Expression ProfilingGene Expression RegulationHumansKeratinocytesMice, Inbred C57BLNeutrophilsPruritusReceptors, CXCR3Sensory Receptor CellscalcipotrieneCalcitriolChemokine CXCL10CytokinesReceptors, CXCR3atopic dermatitischronic itchimmunologyinflammationitchmouseneuroimmuneneuroscienceneutrophilssomatosensory

Identifiers

PMID31631836
PMCPMC6884397
OpenAlexW2982274710

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.