Evidence map›Paper›PMID 17885690›Full record

ArticleThe Journal of clinical investigation2007

IL-13Ralpha2 and IL-10 coordinately suppress airway inflammation, airway-hyperreactivity, and fibrosis in mice.

Mark S Wilson, Eldad Elnekave, Margaret M Mentink-Kane, Marcus G Hodges, John T Pesce, Thirumalai R Ramalingam, Robert W Thompson, Masahito Kamanaka, Richard A Flavell, Andrea Keane-Myers and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.

0numbers the graph read from it
0cells of the map it votes in
79citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

79 citing papers in PubMed, 139 citations in OpenAlex.

  1. Effect of Xinjiang UyghurBioMed research international · 2016
    Trial
  2. Trial
  3. Article
  4. Article
  5. T Regulatory Mechanisms in Airway and Interstitial Lung Disease.Seminars in respiratory and critical care medicine · 2025
    Review
  6. Article
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  9. Article
  10. Article
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  12. Article
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  15. Article
  16. Review
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  19. IL-10 as a Th2 Cytokine: Differences Between Mice and Humans.Journal of immunology (Baltimore, Md. : 1950) · 2021
    Review
  20. Article

19 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

12 authors at 2 institutions in 1 country.

Mark S WilsonImmunopathogenesis Section, Laboratory of Parasitic Diseases, and Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases (NIAID), NIH, Bethesda, Maryland, USA.
Eldad Elnekave
Margaret M Mentink-Kane
Marcus G Hodges
John T Pesce
Thirumalai R Ramalingam
Robert W Thompson
Masahito Kamanaka
Richard A Flavell
Andrea Keane-Myers
Allen W Cheever
Thomas A Wynn
Yale University · USBiomedical Research Institute · US

Funding

Intramural NIH HHS
6 · The paper itself

Abstract

Development of persistent Th2 responses in asthma and chronic helminth infections are a major health concern. IL-10 has been identified as a critical regulator of Th2 immunity, but mechanisms for controlling Th2 effector function remain unclear. IL-10 also has paradoxical effects on Th2-associated pathology, with IL-10 deficiency resulting in increased Th2-driven inflammation but also reduced airway hyperreactivity (AHR), mucus hypersecretion, and fibrosis. We demonstrate that increased IL-13 receptor alpha 2 (IL-13Ralpha2) expression is responsible for the reduced AHR, mucus production, and fibrosis in BALB/c IL-10(-/-) mice. Using models of allergic asthma and chronic helminth infection, we demonstrate that IL-10 and IL-13Ralpha2 coordinately suppress Th2-mediated inflammation and pathology, respectively. Although IL-10 was identified as the dominant antiinflammatory mediator, studies with double IL-10/IL-13Ralpha2-deficient mice illustrate an indispensable role for IL-13Ralpha2 in the suppression of AHR, mucus production, and fibrosis. Thus, IL-10 and IL-13Ralpha2 are both required to control chronic Th2-driven pathological responses.

Indexed as

AnimalsAsthmaBronchial HyperreactivityBronchitisFibrosisGranulomaInterleukin-10Interleukin-13 Receptor alpha2 SubunitMiceMice, Mutant StrainsMucusTh1 CellsTh2 CellsInterleukin-10Interleukin-13 Receptor alpha2 Subunit

Identifiers

PMID17885690
PMCPMC1978425
OpenAlexW2135565397

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.