Evidence map›Paper›PMID 25932692›Full record

ArticlePain2015

CXCR3 chemokine receptor signaling mediates itch in experimental allergic contact dermatitis.

Lintao Qu, Kai Fu, Jennifer Yang, Steven G Shimada, Robert H LaMotte

Open access · greenAbstract read
In one paragraph

Article in Pain, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
6.6field-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

35 citing papers in PubMed, 86 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Neutrophils in Atopic Dermatitis.Clinical reviews in allergy & immunology · 2024
    Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Critical Players and Therapeutic Targets in Chronic Itch.International journal of molecular sciences · 2022
    Review
  12. TRPC3 Antagonizes Pruritus in a Mouse Contact Dermatitis Model.The Journal of investigative dermatology · 2022
    Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Physiology and Pathophysiology of Itch.Physiological reviews · 2020
    Review
  19. Mechanisms and Management of Itch in Dry Skin.Acta dermato-venereologica · 2020
    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

5 authors at 2 institutions in 1 country.

Lintao QuDepartment of Anesthesiology, Yale University School of Medicine, New Haven, CT, USA Department of Neurosurgery, Neurosurgery Pain Research Institute, Johns Hopkins School of Medicine, Baltimore, MD, USA Department of Genetics, Yale University School of Medicine, New Haven, CT, USA.
Kai Fu
Jennifer Yang
Steven G Shimada
Robert H LaMotte
Yale University · USJohns Hopkins Medicine · US

Funding

Research Project CoreP01NS047399 · NINDS · YALE UNIVERSITY · PI LA MOTTE, ROBERT H · 2004 to 2013
$11.0M
Peripheral Neural Mechanisms of Inflammatory Itch and PainR01NS014624 · NINDS · YALE UNIVERSITY · PI LA MOTTE, ROBERT H · 1985 to 2016
$7.2M
Canadian Institutes of Health ResearchNINDS NIH HHS NS014624NINDS NIH HHS NS047399NINDS NIH HHS P01 NS047399NINDS NIH HHS R01 NS014624
6 · The paper itself

Abstract

Persistent itch is a common symptom of allergic contact dermatitis (ACD) and represents a significant health burden. The chemokine CXCL10 is predominantly produced by epithelial cells during ACD. Although the chemokine CXCL10 and its receptor CXCR3 are implicated in the pathophysiology of ACD, it is largely unexplored for itch and pain accompanying this disorder. Here, we showed that CXCL10 and CXCR3 mRNA, protein, and signaling activity were upregulated in the dorsal root ganglion after contact hypersensitivity (CHS), a murine model of ACD, induced by squaric acid dibutylester. CXCL10 directly activated a subset of cutaneous dorsal root ganglion neurons innervating the area of CHS through neuronal CXCR3. In behavioral tests, a CXCR3 antagonist attenuated spontaneous itch- but not pain-like behaviors directed to the site of CHS. Injection of CXCL10 into the site of CHS elicited site-directed itch- but not pain-like behaviors, but neither type of CXCL10-evoked behaviors was observed in control mice. These results suggest that CXCL10/CXCR3 signaling mediates allergic itch but not inflammatory pain in the context of skin inflammation. Thus, upregulation of CXCL10/CXCR3 signaling in sensory neurons may contribute to itch associated with ACD. Targeting the CXCL10/CXCR3 signaling might be beneficial for the treatment of allergic itch.

Indexed as

AcetamidesAnimalsAnti-Allergic AgentsCells, CulturedChemokine CXCL10Dermatitis, Allergic ContactDisease Models, AnimalGanglia, SpinalMaleMembrane PotentialsMiceMice, Inbred C57BLNeuronsPruritusPyrimidinonesReceptors, CXCR3AcetamidesAnti-Allergic AgentsChemokine CXCL10Cxcl10 protein, mouseCxcr3 protein, mouseMrgprA3 protein, mouseMrgprd protein, mouseN-(1-(3-(4-ethoxyphenyl)-4-oxo-3,4-dihydropyrido(2,3-d)pyrimidin-2-yl)ethyl)-N-pyridin-3-ylmethyl-2-(4-trifluoromethoxyphenyl)acetamidePyrimidinonesReceptors, CXCR3Receptors, G-Protein-Coupled

Identifiers

PMID25932692
PMCPMC4545682
OpenAlexW2041373750

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.