Evidence map›Paper›PMID 22005301›Full record

ArticleThe Journal of clinical investigation2011

The protective role of TLR6 in a mouse model of asthma is mediated by IL-23 and IL-17A.

Ana Paula Moreira, Karen A Cavassani, Ugur B Ismailoglu, Rikki Hullinger, Michael P Dunleavy, Darryl A Knight, Steven L Kunkel, Satoshi Uematsu, Shizuo Akira, Cory M Hogaboam

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
6.9field-weighted citation impact, top 2% 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

42 citing papers in PubMed, 83 citations in OpenAlex.

  1. Review
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  12. TRAIL-Dependent Resolution of Pulmonary Fibrosis.Mediators of inflammation · 2018
    Article
  13. Review
  14. Review
  15. Lack of autophagy induces steroid-resistant airway inflammation.The Journal of allergy and clinical immunology · 2016
    Article
  16. Review
  17. Article
  18. Article
  19. Expression of Toll-like receptors in nasal epithelium in allergic rhinitis.APMIS : acta pathologica, microbiologica, et immunologica Scandinavica · 2015
    Article
  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

10 authors at 3 institutions in 3 countries.

Ana Paula MoreiraDepartment of Pathology, University of Michigan Medical School, Ann Arbor, Michigan, USA. anapaula@umich.edu
Karen A Cavassani
Ugur B Ismailoglu
Rikki Hullinger
Michael P Dunleavy
Darryl A Knight
Steven L Kunkel
Satoshi Uematsu
Shizuo Akira
Cory M Hogaboam
University of Michigan · USThe University of Osaka · JPUniversity of British Columbia · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

TLRs are a family of receptors that mediate immune system pathogen recognition. In the respiratory system, TLR activation has both beneficial and deleterious effects in asthma. For example, clinical data indicate that TLR6 activation exerts protective effects in asthma. Here, we explored the mechanism or mechanisms through which TLR6 mediates this effect using mouse models of Aspergillus fumigatus-induced and house dust mite antigen-induced (HDM antigen-induced) chronic asthma. Tlr6-/- mice with fungal- or HDM antigen-induced asthma exhibited substantially increased airway hyperresponsiveness, inflammation, and remodeling compared with WT asthmatic groups. Surprisingly, whole-lung levels of IL-23 and IL-17 were markedly lower in Tlr6-/- versus WT asthmatic mice. Tlr6-/- DCs generated less IL-23 upon activation with lipopolysaccharide, zymosan, or curdlan. Impaired IL-23 generation in Tlr6-/- mice also corresponded with lower levels of expression of the pathogen-recognition receptor dectin-1 and expansion of Th17 cells both in vivo and in vitro. Exogenous IL-23 treatment of asthmatic Tlr6-/- mice restored IL-17A production and substantially reduced airway hyperresponsiveness, inflammation, and lung fungal burden compared with that in untreated asthmatic Tlr6-/- mice. Together, our data demonstrate that TLR6 activation is critical for IL-23 production and Th17 responses, which both regulate the allergic inflammatory response in chronic fungal-induced asthma. Thus, therapeutics targeting TLR6 activity might prove efficacious in the treatment of clinical asthma.

Indexed as

Airway ResistanceAnimalsAspergillus fumigatusAsthmaDendritic CellsDisease Models, AnimalFemaleHumansInterleukin-17Interleukin-23 Subunit p19MiceMice, Inbred C57BLMice, KnockoutModels, ImmunologicalPyroglyphidaeReceptors, Pattern RecognitionIl17a protein, mouseIl23a protein, mouseInterleukin-17Interleukin-23 Subunit p19Receptors, Pattern RecognitionTLR6 protein, humanTlr6 protein, mouseToll-Like Receptor 6

Identifiers

PMID22005301
PMCPMC3204826
OpenAlexW2109672256

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.