Evidence map›Paper›PMID 19060952›Full record

ArticlePloS one2008

Allergen uptake, activation, and IL-23 production by pulmonary myeloid DCs drives airway hyperresponsiveness in asthma-susceptible mice.

Ian P Lewkowich, Stephane Lajoie, Jennifer R Clark, Nancy S Herman, Alyssa A Sproles, Marsha Wills-Karp

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
5.5field-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

63 citing papers in PubMed, 98 citations in OpenAlex.

  1. Article
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  13. Dendritic Cells: Critical Regulators of Allergic Asthma.International journal of molecular sciences · 2020
    Review
  14. Article
  15. Resolvin E3 attenuates allergic airway inflammationFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Article
  16. Combined administration of anti-IL-13 and anti-IL-17A at individually sub-therapeutic doses limits asthma-like symptoms in a mouse model of Th2/Th17 high asthma.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2019
    Article
  17. Article
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  20. Pentraxin 3 deletion aggravates allergic inflammation through a TThe Journal of allergy and clinical immunology · 2017
    Article

3 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

6 authors at 2 institutions in 1 country.

Ian P LewkowichDivision of Immunobiology, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, Ohio, United States of America.
Stephane Lajoie
Jennifer R Clark
Nancy S Herman
Alyssa A Sproles
Marsha Wills-Karp
Cincinnati Children's Hospital Medical Center · USUniversity of Cincinnati · US

Funding

Unique Effects of IL-13 in Asthma: Mechanistic AnalysisP01HL076383 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI ROTHENBERG, MARC E. · 2004 to 2008
$10.1M
ROLE OF ANGPTL4, AN ANGIOGENIC MEDIATOR, IN ARTHRITISP30AR047363 · NIAMS · CINCINNATI CHILDRENS HOSP MED CTR · PI THOMPSON, SUSAN D · 2001 to 2015
$9.2M
Asthma Positional Candidate Genes in Mice and HumansR01HL067736 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI WILLS-KARP, MARSHA · 2000 to 2010
$4.1M
Epithelial Regulation of Th2 Immune Responses in the LungR01AI083315 · NIAID · JOHNS HOPKINS UNIVERSITY · PI WILLS-KARP, MARSHA · 2009 to 2013
$1.9M
NHLBI NIH HHS HL076383NHLBI NIH HHS HL67736NHLBI NIH HHS P01 HL076383NHLBI NIH HHS R01 HL067736NIAID NIH HHS R01 AI083315NIAMS NIH HHS AR47363NIAMS NIH HHS P30 AR047363
6 · The paper itself

Abstract

Maladaptive, Th2-polarized inflammatory responses are integral to the pathogenesis of allergic asthma. As regulators of T cell activation, dendritic cells (DCs) are important mediators of allergic asthma, yet the precise signals which render endogenous DCs "pro-asthmatic", and the extent to which these signals are regulated by the pulmonary environment and host genetics, remains unclear. Comparative phenotypic and functional analysis of pulmonary DC populations in mice susceptible (A/J), or resistant (C3H) to experimental asthma, revealed that susceptibility to airway hyperresponsiveness is associated with preferential myeloid DC (mDC) allergen uptake, and production of Th17-skewing cytokines (IL-6, IL-23), whereas resistance is associated with increased allergen uptake by plasmacytoid DCs. Surprisingly, adoptive transfer of syngeneic HDM-pulsed bone marrow derived mDCs (BMDCs) to the lungs of C3H mice markedly enhanced lung IL-17A production, and rendered them susceptible to allergen-driven airway hyperresponsiveness. Characterization of these BMDCs revealed levels of antigen uptake, and Th17 promoting cytokine production similar to that observed in pulmonary mDCs from susceptible A/J mice. Collectively these data demonstrate that the lung environment present in asthma-resistant mice promotes robust pDC allergen uptake, activation, and limits Th17-skewing cytokine production responsible for driving pathologic T cell responses central to the development of allergen-induced airway hyperresponsiveness.

Indexed as

Adoptive TransferAllergensAnimalsAsthmaBone Marrow CellsBronchial HyperreactivityDendritic CellsDisease Models, AnimalDisease SusceptibilityInterleukin-17Interleukin-23LungLymph NodesMiceMice, Inbred C3HMyeloid CellsAllergensInterleukin-17Interleukin-23

Identifiers

PMID19060952
PMCPMC2586658
OpenAlexW2062367951

What OpenQuestion holds

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LicenceCC BY
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.