Evidence map›Paper›PMID 26290411›Full record

ArticleScience translational medicine2015

TH2 and TH17 inflammatory pathways are reciprocally regulated in asthma.

David F Choy, Kevin M Hart, Lee A Borthwick, Aarti Shikotra, Deepti R Nagarkar, Salman Siddiqui, Guiquan Jia, Chandra M Ohri, Emma Doran, Kevin M Vannella and 15 more

Open access · greenAbstract read
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In one paragraph

Article in Science translational medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 267 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
267citing papers in PubMed, 4 pooled it
27.5field-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

267 citing papers in PubMed, 4 syntheses or guidelines pooled it, 440 citations in OpenAlex.

  1. Pooled it
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  14. Mechanisms and therapeutic strategies of asthma: from bench to bedside.Signal transduction and targeted therapy · 2026
    Review
  15. Article
  16. Persistent exposure to second-hand smoke and asthma endotypes in a study of Puerto Rican youth.Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology · 2026
    Article
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207 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

25 authors at 3 institutions in 2 countries.

David F ChoyGenentech Inc., South San Francisco, CA 94080, USA.
Kevin M HartProgram in Tissue Immunity and Repair, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
Lee A BorthwickTissue Fibrosis and Repair Group, Institute of Cellular Medicine, Newcastle University, Newcastle upon Tyne NE2 4HH, UK.
Aarti ShikotraInstitute for Lung Health, Department of Infection, Immunity and Inflammation, University of Leicester, Leicester LE3 9QP, UK.
Deepti R NagarkarGenentech Inc., South San Francisco, CA 94080, USA.
Salman SiddiquiInstitute for Lung Health, Department of Infection, Immunity and Inflammation, University of Leicester, Leicester LE3 9QP, UK.
Guiquan JiaGenentech Inc., South San Francisco, CA 94080, USA.
Chandra M OhriInstitute for Lung Health, Department of Infection, Immunity and Inflammation, University of Leicester, Leicester LE3 9QP, UK.
Emma DoranGenentech Inc., South San Francisco, CA 94080, USA. Centre for Infection and Immunity, Health Sciences Building, Queens University Belfast, Lisburn Road, Belfast BT9 7AB, Northern Ireland, UK.
Kevin M VannellaProgram in Tissue Immunity and Repair, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
Claire A ButlerCentre for Infection and Immunity, Health Sciences Building, Queens University Belfast, Lisburn Road, Belfast BT9 7AB, Northern Ireland, UK.
Beverley HargadonInstitute for Lung Health, Department of Infection, Immunity and Inflammation, University of Leicester, Leicester LE3 9QP, UK.
Joshua C SciurbaProgram in Tissue Immunity and Repair, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
Richard L GieseckProgram in Tissue Immunity and Repair, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
Robert W ThompsonProgram in Tissue Immunity and Repair, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
Sandra WhiteProgram in Tissue Immunity and Repair, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
Alexander R AbbasGenentech Inc., South San Francisco, CA 94080, USA.
Janet JackmanGenentech Inc., South San Francisco, CA 94080, USA.
Lawren C WuGenentech Inc., South San Francisco, CA 94080, USA.
Jackson G EgenGenentech Inc., South San Francisco, CA 94080, USA.
Liam G HeaneyCentre for Infection and Immunity, Health Sciences Building, Queens University Belfast, Lisburn Road, Belfast BT9 7AB, Northern Ireland, UK.
Thirumalai R RamalingamProgram in Tissue Immunity and Repair, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
Joseph R ArronGenentech Inc., South San Francisco, CA 94080, USA. arron.joseph@gene.com.
Thomas A WynnProgram in Tissue Immunity and Repair, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
Peter BraddingInstitute for Lung Health, Department of Infection, Immunity and Inflammation, University of Leicester, Leicester LE3 9QP, UK.
University of Leicester · GBNational Institute of Allergy and Infectious Diseases · USNational Institutes of Health · US

Funding

Intramural NIH HHS
6 · The paper itself

Abstract

Increasing evidence suggests that asthma is a heterogeneous disorder regulated by distinct molecular mechanisms. In a cross-sectional study of asthmatics of varying severity (n = 51), endobronchial tissue gene expression analysis revealed three major patient clusters: TH2-high, TH17-high, and TH2/17-low. TH2-high and TH17-high patterns were mutually exclusive in individual patient samples, and their gene signatures were inversely correlated and differentially regulated by interleukin-13 (IL-13) and IL-17A. To understand this dichotomous pattern of T helper 2 (TH2) and TH17 signatures, we investigated the potential of type 2 cytokine suppression in promoting TH17 responses in a preclinical model of allergen-induced asthma. Neutralization of IL-4 and/or IL-13 resulted in increased TH17 cells and neutrophilic inflammation in the lung. However, neutralization of IL-13 and IL-17 protected mice from eosinophilia, mucus hyperplasia, and airway hyperreactivity and abolished the neutrophilic inflammation, suggesting that combination therapies targeting both pathways may maximize therapeutic efficacy across a patient population comprising both TH2 and TH17 endotypes.

Indexed as

AnimalsAsthmaCells, CulturedFemaleHumansInterleukin-13Interleukin-17MiceMice, Inbred BALB CSignal TransductionTh17 CellsTh2 CellsInterleukin-13Interleukin-17

Identifiers

PMID26290411
OpenAlexW2166997969

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.