Evidence map›Paper›PMID 26299987›Full record

ArticleThe Journal of allergy and clinical immunology2016

Spontaneous atopic dermatitis is mediated by innate immunity, with the secondary lung inflammation of the atopic march requiring adaptive immunity.

Sean P Saunders, Tara Moran, Achilleas Floudas, Felicity Wurlod, Agnieszka Kaszlikowska, Maryam Salimi, Emma M Quinn, Christopher J Oliphant, Gabriel Núñez, Ross McManus and 5 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of allergy and clinical immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
16.4field-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

59 citing papers in PubMed, 160 citations in OpenAlex.

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  6. Biomaterials research · 2025
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  20. Revisiting the Roles of Filaggrin in Atopic Dermatitis.International journal of molecular sciences · 2022
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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

15 authors at 9 institutions in 3 countries.

Sean P SaundersTrinity Biomedical Sciences Institute, Trinity College Dublin, Dublin, Ireland; National Children's Research Centre, Our Lady's Children's Hospital, Dublin, Ireland.
Tara MoranTrinity Biomedical Sciences Institute, Trinity College Dublin, Dublin, Ireland; National Children's Research Centre, Our Lady's Children's Hospital, Dublin, Ireland.
Achilleas FloudasTrinity Biomedical Sciences Institute, Trinity College Dublin, Dublin, Ireland; National Children's Research Centre, Our Lady's Children's Hospital, Dublin, Ireland.
Felicity WurlodTrinity Biomedical Sciences Institute, Trinity College Dublin, Dublin, Ireland; National Children's Research Centre, Our Lady's Children's Hospital, Dublin, Ireland.
Agnieszka KaszlikowskaTrinity Biomedical Sciences Institute, Trinity College Dublin, Dublin, Ireland; National Children's Research Centre, Our Lady's Children's Hospital, Dublin, Ireland.
Maryam SalimiMRC Human Immunology Unit, NIHR Biomedical Research Centre, Radcliffe Department of Medicine, University of Oxford, Oxford, United Kingdom.
Emma M QuinnInstitute of Molecular Medicine, St James's Hospital, Dublin, Ireland.
Christopher J OliphantMRC Laboratory of Molecular Biology, Cambridge, United Kingdom; Biosceptre, Babraham Research Campus, Babraham, Cambridge, United Kingdom.
Gabriel NúñezDepartment of Pathology and Comprehensive Cancer Center, University of Michigan, Ann Arbor, Mich.
Ross McManusInstitute of Molecular Medicine, St James's Hospital, Dublin, Ireland.
Emily HamsTrinity Biomedical Sciences Institute, Trinity College Dublin, Dublin, Ireland; National Children's Research Centre, Our Lady's Children's Hospital, Dublin, Ireland.
Alan D IrvineNational Children's Research Centre, Our Lady's Children's Hospital, Dublin, Ireland; Department of Paediatric Dermatology, Our Lady's Children's Hospital, Dublin, Ireland.
Andrew N J McKenzieMRC Laboratory of Molecular Biology, Cambridge, United Kingdom.
Graham S OggMRC Human Immunology Unit, NIHR Biomedical Research Centre, Radcliffe Department of Medicine, University of Oxford, Oxford, United Kingdom.
Padraic G FallonTrinity Biomedical Sciences Institute, Trinity College Dublin, Dublin, Ireland; National Children's Research Centre, Our Lady's Children's Hospital, Dublin, Ireland; Institute of Molecular Medicine, St James's Hospital, Dublin, Ireland. Electronic address: pfallon@tcd.ie.
National Children’s Research Centre · IESt. James's Hospital · IETrinity College Dublin · IEBabraham Bioscience Technologies (United Kingdom) · GBMRC Human Immunology Unit · GBMRC Laboratory of Molecular Biology · GBOur Lady's Hospital · IEOxford BioMedica (United Kingdom) · GBUniversity of Michigan–Ann Arbor · US

Funding

Medical Research Council MC_U105178805Medical Research Council MC_UU_12010/5Wellcome Trust 092530/Z/10/Z
6 · The paper itself

Abstract

backgroundAtopic dermatitis (AD) is an inflammatory skin condition that can occur in early life, predisposing to asthma development in a phenomenon known as the atopic march. Although genetic and environmental factors are known to contribute to AD and asthma, the mechanisms underlying the atopic march remain poorly understood. Filaggrin loss-of-function mutations are a major genetic predisposer for the development of AD and progression to AD-associated asthma.

objectiveWe sought to experimentally address whether filaggrin mutations in mice lead to the development of spontaneous eczematous inflammation and address the aberrant immunologic milieu arising in a mouse model of filaggrin deficiency.

methodsFilaggrin mutant mice were generated on the proallergic BALB/c background, creating a novel model for the assessment of spontaneous AD-like inflammation. Independently recruited AD case collections were analyzed to define associations between filaggrin mutations and immunologic phenotypes.

resultsFilaggrin-deficient mice on a BALB/c background had profound spontaneous AD-like inflammation with progression to compromised pulmonary function with age, reflecting the atopic march in patients with AD. Strikingly, skin inflammation occurs independently of adaptive immunity and is associated with cutaneous expansion of IL-5-producing type 2 innate lymphoid cells. Furthermore, subjects with filaggrin mutations have an increased frequency of type 2 innate lymphoid cells in the skin in comparison with control subjects.

conclusionThis study provides new insights into our understanding of the atopic march, with innate immunity initiating dermatitis and the adaptive immunity required for subsequent development of compromised lung function.

Indexed as

Adaptive ImmunityImmunity, InnateAnimalsDermatitis, AtopicDisease Models, AnimalFilaggrin ProteinsIntermediate Filament ProteinsLymphocytesMiceMice, TransgenicMutationPhenotypePneumoniaSkinFilaggrin ProteinsFLG protein, humanIntermediate Filament ProteinsAllergyasthmaatopic dermatitisatopyeczemafilaggrinflaky tailinnate immunitymousemutationtype 2 innate lymphoid cells

Identifiers

PMID26299987
PMCPMC4735016
OpenAlexW1167372180

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.