Evidence map›Paper›PMID 11514610›Full record

ArticleThe Journal of experimental medicine2001

Requirement for the chemokine receptor CCR6 in allergic pulmonary inflammation.

N W Lukacs, D M Prosser, M Wiekowski, S A Lira, D N Cook

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

38 citing papers in PubMed, 139 citations in OpenAlex.

  1. Observational
  2. Article
  3. TFrontiers in immunology · 2022
    Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. CARMA3 Is Critical for the Initiation of Allergic Airway Inflammation.Journal of immunology (Baltimore, Md. : 1950) · 2015
    Article
  11. Article
  12. Article
  13. CCL20/MIP-3 alpha mRNA expression in the conjunctival epithelium of normal individuals and patients with vernal keratoconjunctivitis.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2014
    Article
  14. Synthetic di-sulfated iduronic acid attenuates asthmatic response by blocking T-cell recruitment to inflammatory sites.Proceedings of the National Academy of Sciences of the United States of America · 2014
    Article
  15. Review
  16. Article
  17. Article
  18. Experimental advances in understanding allergic airway inflammation.Frontiers in bioscience (Scholar edition) · 2013
    Review
  19. 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 1 institution in 1 country.

N W LukacsDepartment of Immunology, Schering-Plough Research Institute, Kenilworth, NJ 07033, USA.
D M Prosser
M Wiekowski
S A Lira
D N Cook
University of Michigan–Ann Arbor · US

Funding

MONONUCLEAR LEUKOCYTE ADHESION AND RECRUITMENT IN CHRONIC INFLAMMATORY DISEASEP01HL031963 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI JOHNSON, KENT JOHN · 1985 to 2009
$14.1M
The Role of C-C Chemokines in Eosinophil Airway InflammationR01AI036302 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI LUKACS, NICHOLAS W · 2001 to 2018
$5.6M
C-C CHEMOKINES AND EOSINOPHIL AIRWAY INFLAMMATIONR29AI036302 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI LUKACS, NICHOLAS W · 1996 to 2000
$107k
NHLBI NIH HHS HL31963NHLBI NIH HHS P01 HL031963NIAID NIH HHS AI36302NIAID NIH HHS R01 AI036302NIAID NIH HHS R29 AI036302
6 · The paper itself

Abstract

Allergic asthmatic responses in the airway are associated with airway hyperreactivity, eosinophil accumulation in the lung, and cytokine production by allergen-specific, T helper cell type 2 (Th2) lymphocytes. Here, we show that in a cockroach antigen (CA) model of allergic pulmonary inflammation, the chemokine macrophage inflammatory protein (MIP)-3alpha is expressed in the lung within hours of allergen challenge. To determine the biologic relevance of this expression, mice lacking CCR6, the only known receptor for MIP-3alpha, were studied for their response to CA. CCR6-deficient mice were immunized to the same extent as their wild-type counterparts, as judged by cytokine production in antigen-challenged lymphocytes. However, compared with CA-challenged wild-type mice, challenged CCR6-deficient mice had reduced airway resistance, fewer eosinophils around the airway, lower levels of interleukin 5 in the lung, and reduced serum levels of immunoglobulin E. Together, these data demonstrate that MIP-3alpha and CCR6 function in allergic pulmonary responses and suggest that these molecules might represent novel therapeutic targets for treatment of asthma.

Indexed as

AnimalsAsthmaCytokinesHypersensitivityImmunoglobulin EMiceMice, Inbred C57BLMice, KnockoutPneumoniaReceptors, CCR6Receptors, ChemokineTh2 CellsCCR6 protein, humanCytokinesImmunoglobulin EReceptors, CCR6Receptors, Chemokine

Identifiers

PMID11514610
PMCPMC2193496
OpenAlexW2126246192

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.