Evidence map›Paper›PMID 25681342›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2015

Cutting edge: STAT6 signaling in eosinophils is necessary for development of allergic airway inflammation.

Kindra Stokes, Nelson M LaMarche, Nasif Islam, Amie Wood, Weishan Huang, Avery August

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

15 citing papers in PubMed, 25 citations in OpenAlex.

  1. Review
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  8. Network Pharmacology-Based Study on the Mechanism ofEvidence-based complementary and alternative medicine : eCAM · 2020
    Article
  9. Article
  10. Review
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  15. Article
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

6 authors at 2 institutions in 1 country.

Kindra StokesPathobiology Graduate Program, Center for Molecular Immunology and Infectious Diseases, Department of Veterinary and Biomedical Sciences, The Pennsylvania State University, University Park, PA 16802; and Department of Microbiology and Immunology, Cornell University, Ithaca, NY 14853.
Nelson M LaMarcheDepartment of Microbiology and Immunology, Cornell University, Ithaca, NY 14853.
Nasif IslamDepartment of Microbiology and Immunology, Cornell University, Ithaca, NY 14853.
Amie WoodDepartment of Microbiology and Immunology, Cornell University, Ithaca, NY 14853.
Weishan HuangDepartment of Microbiology and Immunology, Cornell University, Ithaca, NY 14853.ORCID http://orcid.org/0000-0002-1330-1131
Avery AugustDepartment of Microbiology and Immunology, Cornell University, Ithaca, NY 14853 averyaugust@cornell.edu.ORCID http://orcid.org/0000-0003-4968-3415
Cornell University · USPennsylvania State University · US

Funding

Eosinophils and Allergic Airway ResponsesR01AI073955 · NIAID · PENNSYLVANIA STATE UNIVERSITY, THE · PI AUGUST, AVERY · 2008 to 2012
$1.9M
Eosinophils and Allergic Airway ResponsesR56AI073955 · NIAID · PENNSYLVANIA STATE UNIVERSITY, THE · PI AUGUST, AVERY · 2008 to 2008
$61k
NIAID NIH HHS AI073955NIAID NIH HHS R01 AI073955NIAID NIH HHS R56 AI073955
6 · The paper itself

Abstract

Eosinophils are critical cellular mediators in allergic asthma and inflammation; however, the signals that regulate their functions are unclear. The transcription factor STAT6 regulates Th2 cytokine responses, acting downstream of IL-4 and IL-13. We showed previously that eosinophil-derived IL-13 plays an important role in the recruitment of T cells to the lung and the subsequent development of allergic asthma. However, whether eosinophils respond to Th2 signals to control allergic airway inflammation is unclear. In this report, we show that STAT6(-/-) eosinophils are unable to induce the development of allergic lung inflammation, including recruitment of CD4(+) T cells, mucus production, and development of airways hyperresponsiveness. This is likely due to the reduced migration of STAT6(-/-) eosinophils to the lung and in response to eotaxin. These data indicate that, like Th cells, eosinophils need to respond to Th2 cytokines via STAT6 during the development of allergic airway inflammation.

Indexed as

AnimalsAsthmaCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesCell MovementCytokinesEosinophilsFlow CytometryInflammationMice, Inbred C57BLMice, KnockoutMice, TransgenicOvalbuminRespiratory HypersensitivitySignal TransductionSTAT6 Transcription FactorCytokinesOvalbuminSTAT6 Transcription Factor

Identifiers

PMID25681342
PMCPMC4470169
OpenAlexW2166335246

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.