Evidence map›Paper›PMID 27417023›Full record

ArticleThe Journal of allergy and clinical immunology2017

IL-17A enhances IL-13 activity by enhancing IL-13-induced signal transducer and activator of transcription 6 activation.

Sara L Hall, Theresa Baker, Stephane Lajoie, Phoebe K Richgels, Yanfen Yang, Jaclyn W McAlees, Adelaide van Lier, Marsha Wills-Karp, Umasundari Sivaprasad, Thomas H Acciani and 4 more

2 registry-linked trialsOpen access · bronzeAbstract read
In one paragraph

Article in The Journal of allergy and clinical immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 2 registered trials, which are not on this map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
4.9field-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.

NCT05623059 phase1 / phase2completednot on this mapstarted 2023, after this paper: background citation

Phase IIa Clinical Trial to Evaluate Pharmacokinetics and Safety of Slow Release DHEA

TypeinterventionalSponsorIndiana UniversityRan2023 to 2025Enrolled18ConditionsAsthma, GenotypeArmsSlow Release DHEA
NCT07179952 phase2not yet recruitingnot on this mapstarted 2027, after this paper: background citation

A Study to Evaluate Efficacy and Safety of Slow Release DHEA

TypeinterventionalSponsorIndiana UniversityRan2027 to 2028Enrolled30ConditionsAsthmaArmsSlow Release DHEA, Placebo
3 · Its place in the literature

Who cites it

52 citing papers in PubMed, 71 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Cytokines Associated with Activation of CD4International journal of molecular sciences · 2026
    Review
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  6. Review
  7. Article
  8. Article
  9. Article
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  11. Review
  12. Article
  13. Delayed Microbial Maturation Durably Exacerbates Th17-driven Asthma in Mice.American journal of respiratory cell and molecular biology · 2023
    Article
  14. Review
  15. Development of Adaptive Immunity and Its Role in Lung Remodeling.Advances in experimental medicine and biology · 2023
    Article
  16. Article
  17. Article
  18. Article
  19. Modulation of IL-4/IL-13 cytokine signaling in the context of allergic disease.The Journal of allergy and clinical immunology · 2022
    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

14 authors at 2 institutions in 1 country.

Sara L HallDivision of Immunobiology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio.
Theresa BakerDivision of Asthma Research, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio.
Stephane LajoieBloomberg School of Public Health, Johns Hopkins University, Baltimore, Md.
Phoebe K RichgelsDivision of Immunobiology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio.
Yanfen YangDivision of Immunobiology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio.
Jaclyn W McAleesDivision of Immunobiology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio.
Adelaide van LierDivision of Immunobiology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio.
Marsha Wills-KarpBloomberg School of Public Health, Johns Hopkins University, Baltimore, Md.
Umasundari SivaprasadDivision of Asthma Research, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio.
Thomas H AccianiDivision of Pulmonary Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio.
Timothy D LeCrasDivision of Pulmonary Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio.
Jocelyn Biagini MyersDivision of Asthma Research, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio.
Melinda Butsch KovacicDivision of Asthma Research, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio.
Ian P LewkowichDivision of Immunobiology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio. Electronic address: Ian.Lewkowich@cchmc.org.
Cincinnati Children's Hospital Medical Center · USJohns Hopkins University · US

Funding

Mechanisms of IL-17A-mediated enhancement of asthma severityR01HL122300 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI LEWKOWICH, IAN PAUL · 2014 to 2018
$2.2M
NHLBI NIH HHS R01 HL122300
6 · The paper itself

Abstract

backgroundIncreased IL-17A production has been associated with more severe asthma; however, the mechanisms whereby IL-17A can contribute to IL-13-driven pathology in asthmatic patients remain unclear.

objectiveWe sought to gain mechanistic insight into how IL-17A can influence IL-13-driven responses.

methodsThe effect of IL-17A on IL-13-induced airway hyperresponsiveness, gene expression, mucus hypersecretion, and airway inflammation was assessed by using in vivo models of IL-13-induced lung pathology and in vitro culture of murine fibroblast cell lines and primary fibroblasts and human epithelial cell lines or primary human epithelial cells exposed to IL-13, IL-17A, or both.

resultsCompared with mice given intratracheal IL-13 alone, those exposed to IL-13 and IL-17A had augmented airway hyperresponsiveness, mucus production, airway inflammation, and IL-13-induced gene expression. In vitro, IL-17A enhanced IL-13-induced gene expression in asthma-relevant murine and human cells. In contrast to the exacerbating influence of IL-17A on IL-13-induced responses, coexposure to IL-13 inhibited IL-17A-driven antimicrobial gene expression in vivo and in vitro. Mechanistically, in both primary human and murine cells, the IL-17A-driven increase in IL-13-induced gene expression was associated with enhanced IL-13-driven signal transducer and activator of transcription 6 activation.

conclusionsOur data suggest that IL-17A contributes to asthma pathophysiology by increasing the capacity of IL-13 to activate intracellular signaling pathways, such as signal transducer and activator of transcription 6. These data represent the first mechanistic explanation of how IL-17A can directly contribute to the pathogenesis of IL-13-driven pathology.

Indexed as

AnimalsAsthmaCell LineCytokinesFibroblastsGene Expression RegulationHumansInterleukin-13Interleukin-13 Receptor alpha2 SubunitInterleukin-17MiceMice, Inbred BALB CMice, KnockoutPneumoniaReceptors, Interleukin-17Signal TransductionCytokinesIl17ra protein, mouseInterleukin-13Interleukin-13 Receptor alpha2 SubunitInterleukin-17Receptors, Interleukin-17STAT6 Transcription FactorAsthmacytokinesIL-13IL-17Asignal transducer and activator of transcription 6signal transduction

Identifiers

PMID27417023
PMCPMC5149451
OpenAlexW2415646315

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

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.