Evidence map›Paper›PMID 11877470›Full record

ArticleThe Journal of clinical investigation2002

CCR3 is essential for skin eosinophilia and airway hyperresponsiveness in a murine model of allergic skin inflammation.

Weilie Ma, Paul J Bryce, Alison A Humbles, Dhafer Laouini, Ali Yalcindag, Harri Alenius, Daniel S Friend, Hans C Oettgen, Craig Gerard, Raif S Geha

Open access · greenAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.

0numbers the graph read from it
0cells of the map it votes in
76citing 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

76 citing papers in PubMed, 244 citations in OpenAlex.

  1. Trial
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  3. Review
  4. Article
  5. CCR3 deficiency shifts adaptive to innate-driven immunity in asthma.The journal of allergy and clinical immunology. Global · 2025
    Article
  6. Review
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  20. IL-22 promotes allergic airway inflammation in epicutaneously sensitized mice.The Journal of allergy and clinical immunology · 2019
    Article

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

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.

Weilie MaDivision of Immunology and Department of Pediatrics, Children's Hospital, Boston, Massachusetts 02115, USA.
Paul J Bryce
Alison A Humbles
Dhafer Laouini
Ali Yalcindag
Harri Alenius
Daniel S Friend
Hans C Oettgen
Craig Gerard
Raif S Geha
Harvard University Press · USENT and Allergy · US

Funding

MOLECULAR BASIS OF ALLERGIC AND IMMUNOLOGIC DISEASET32AI007512 · NIAID · CHILDREN'S HOSPITAL BOSTON · PI Janet Chou, Peter A Nigrovic · 1996 to 2026
$13.1M
IMMUNOLOGIC MECHANISMS OF ATOPIC DERMATITISR01AR047417 · NIAMS · CHILDREN'S HOSPITAL BOSTON · PI GEHA, RAIF SALIM · 2001 to 2011
$3.5M
NIAID NIH HHS T32 AI007512NIAID NIH HHS T32-AI07512NIAMS NIH HHS AR47417NIAMS NIH HHS R01 AR047417
6 · The paper itself

Abstract

The CC chemokine receptor 3 (CCR3) is expressed by eosinophils, mast cells, and Th2 cells. We used CCR3(-/-) mice to assess the role of CCR3 in a murine model of allergic skin inflammation induced by repeated epicutaneous sensitization with ovalbumin (OVA), and characterized by eosinophil skin infiltration, local expression of Th2 cytokines, and airway hyperresponsiveness (AHR) to inhaled antigen. Eosinophils and the eosinophil product major basic protein were absent from the skin of sham and OVA-sensitized CCR3(-/-) mice. Mast cell numbers and expression of IL-4 mRNA were normal in skin of CCR3(-/-) mice, suggesting that CCR3 is not important for infiltration of the skin by mast cells and Th2 cells. CCR3(-/-) mice produced normal levels of OVA-specific IgE, and their splenocytes secreted normal amounts of IL-4 and IL-5 following in vitro stimulation with OVA, indicating effective generation of systemic Th2 helper responses. Recruitment of eosinophils to lung parenchyma and bronchoalveolar lavage (BAL) fluid was severely impaired in CCR3(-/-) mice, which failed to develop AHR to methacholine following antigen inhalation. These results suggest that CCR3 plays an essential role in eosinophil recruitment to the skin and the lung and in the development of AHR.

Indexed as

AnimalsDermatitis, AtopicDisease Models, AnimalEosinophiliaEosinophilsFemaleHumansImmunoglobulin EInterleukin-4Interleukin-5Mast CellsMiceMice, Inbred BALB CMice, KnockoutOvalbuminReceptors, CCR3CCR3 protein, humanCcr3 protein, mouseImmunoglobulin EInterleukin-4Interleukin-5OvalbuminReceptors, CCR3Receptors, Chemokine

Identifiers

PMID11877470
PMCPMC150891
OpenAlexW2084851155

What OpenQuestion holds

Textmetadata
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.