Evidence map›Paper›PMID 27112462›Full record

ArticleRespiratory research2016

CD4⁺ and CD8⁺ T cells play a central role in a HDM driven model of allergic asthma.

Kristof Raemdonck, Katie Baker, Nicole Dale, Eric Dubuis, Fisnik Shala, Maria G Belvisi, Mark A Birrell

Open access · goldAbstract read
In one paragraph

Article in Respiratory research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

32 citing papers in PubMed, 57 citations in OpenAlex.

  1. Ovarian hormones and obesity drive Th17-mediated airway inflammation through estrogen receptor-α signaling.American journal of physiology. Lung cellular and molecular physiology · 2026
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  6. Type-2 CD8Nature communications · 2023
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  8. Production ofJournal of immunology research · 2023
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  9. T-cell responses in asthma exacerbations.Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology · 2022
    Review
  10. Article
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  12. Review
  13. Article
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  15. Observational
  16. Article
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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

7 authors at 3 institutions in 2 countries.

Kristof RaemdonckDivision of Airway Disease, Respiratory Pharmacology, National Heart & Lung Institute, Faculty of Medicine, Imperial College London, Exhibition Road, London, SW7 2AZ, UK.
Katie BakerDivision of Airway Disease, Respiratory Pharmacology, National Heart & Lung Institute, Faculty of Medicine, Imperial College London, Exhibition Road, London, SW7 2AZ, UK.
Nicole DaleDivision of Airway Disease, Respiratory Pharmacology, National Heart & Lung Institute, Faculty of Medicine, Imperial College London, Exhibition Road, London, SW7 2AZ, UK.
Eric DubuisDivision of Airway Disease, Respiratory Pharmacology, National Heart & Lung Institute, Faculty of Medicine, Imperial College London, Exhibition Road, London, SW7 2AZ, UK.
Fisnik ShalaDivision of Airway Disease, Respiratory Pharmacology, National Heart & Lung Institute, Faculty of Medicine, Imperial College London, Exhibition Road, London, SW7 2AZ, UK.
Maria G BelvisiDivision of Airway Disease, Respiratory Pharmacology, National Heart & Lung Institute, Faculty of Medicine, Imperial College London, Exhibition Road, London, SW7 2AZ, UK.
Mark A BirrellDivision of Airway Disease, Respiratory Pharmacology, National Heart & Lung Institute, Faculty of Medicine, Imperial College London, Exhibition Road, London, SW7 2AZ, UK. m.birrell@imperial.ac.uk.
Imperial College London · GBAsthma UK · GBCentre for Health Technology and Services Research · PT

Funding

Biotechnology and Biological Sciences Research Council BB/E52708X/1Medical Research Council MR/K020293/1
6 · The paper itself

Abstract

backgroundThe incidence of asthma is increasing at an alarming rate and while the current available therapies are effective in the majority of patients they fail to adequately control symptoms at the more severe end of the disease spectrum. In the search to understand disease pathogenesis and find effective therapies animal models are often employed. As exposure to house dust mite (HDM) has a causative link, it is thought of as the allergen of choice for modelling asthma. The objective was to develop a HDM driven model of asthmatic sensitisation and characterise the role of key allergic effector cells/mediators.

methodsMice were sensitised with low doses of HDM and then subsequently challenged. Cellular inflammation, IgE and airway responsiveness (AHR) was assessed in wild type mice or CD4(+)/CD8(+) T cells, B cells or IgE knock out mice.

resultsOnly those mice sensitised with HDM responded to subsequent low dose topical challenge. Similar to the classical ovalbumin model, there was no requirement for systemic alum sensitisation. Characterisation of the role of effector cells demonstrated that the allergic cellular inflammation and AHR was dependent on CD4(+) and CD8(+) T cells but not B cells or IgE. Finally, we show that this model, unlike the classic OVA model, appears to be resistant to developing tolerance.

conclusionsThis CD4(+)/CD8(+) T cell dependent, HDM driven model of allergic asthma exhibits key features of asthma. Furthermore, we suggest that the ability to repeat challenge with HDM means this model is amenable to studies exploring the effect of therapeutic dosing in chronic, established disease.

Indexed as

Disease Models, AnimalAnimalsAntigens, DermatophagoidesAsthmaCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesCells, CulturedMaleMiceMice, Inbred C57BLMice, KnockoutPyroglyphidaeRespiratory HypersensitivityAntigens, DermatophagoidesAnimal modelAsthmaInflammationLungT cells

Identifiers

PMID27112462
PMCPMC4845490
OpenAlexW2344773824

What OpenQuestion holds

Textmetadata
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.