ArticleAllergy2019
Spontaneous atopic dermatitis in mice with a defective skin barrier is independent of ILC2 and mediated by IL-1β.
Article in Allergy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
What it found
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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.
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.
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Who cites it
35 citing papers in PubMed, 81 citations in OpenAlex.
- Dermal fibroblasts respond to IL-4 and IL-13 and promote T cell recruitment in atopic dermatitis.The Journal of clinical investigation · 2026Article
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- [Patterns and mechanisms of theZhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2025Article
- In Vitro and in Vivo Efficacy of Different Ointment Formulations ContainingPharmaceuticals (Basel, Switzerland) · 2025Article
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- Conversation between skin microbiota and the host: from early life to adulthood.Experimental & molecular medicine · 2025Review
- Decreased GATA3 levels cause changed mouse cutaneous innate lymphoid cell fate, facilitating hair follicle recycling.Developmental cell · 2024Article
- Immune-Modulating Effects of Low-Carbohydrate Ketogenic Foods in Healthy Canines.Current developments in nutrition · 2024Article
- Preclinical Models of Atopic Dermatitis Suitable for Mechanistic and Therapeutic Investigations.Journal of inflammation research · 2024Review
- NLRP3 deficiency aggravated DNFB-induced chronic itch by enhancing type 2 immunity IL-4/TSLP-TRPA1 axis in mice.Frontiers in immunology · 2024Article
- Gu-Ben-Hua-Shi (AESS) formula ameliorates atopic dermatitis via regulating NLRP3 signaling pathways.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2023Article
- INFRAFRONTIER: mouse model resources for modelling human diseases.Mammalian genome : official journal of the International Mammalian Genome Society · 2023Review
- Challenges and Future Trends in Atopic Dermatitis.International journal of molecular sciences · 2023Review
- Construction and verification of atopic dermatitis diagnostic model based on pyroptosis related biological markers using machine learning methods.BMC medical genomics · 2023Article
- Human umbilical cord mesenchymal stem cell treatment alleviates symptoms in an atopic dermatitis-like mouse model.Stem cell research & therapy · 2023Article
- Potential Role of Innate Lymphoid Cells in the Pathogenesis and Treatment of Skin Diseases.Journal of clinical medicine · 2023Review
- Obesity and the microbiome in atopic dermatitis: Therapeutic implications for PPAR-γ agonists.Frontiers in allergy · 2023Review
- Genomic control of inflammation in experimental atopic dermatitis.Scientific reports · 2022Article
- Context-dependent function of TSLP and IL-1β in skin allergic sensitization and atopic march.Nature communications · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 7 institutions in 6 countries.
Funding
Abstract
backgroundAtopic dermatitis (AD) is one of the most common skin diseases with a multifactorial etiology. Mutations leading to loss of skin barrier function are associated with the development of AD with group 2 innate lymphoid cells (ILC2) promoting acute skin inflammation. Filaggrin-mutant (Flg
methodsMice with a frameshift mutation in the filaggrin gene develop spontaneous dermatitis. Flg
resultsWild-type and Flg
conclusionsIn summary, we identified a critical role for the microbiome and IL-1β mediating chronic inflammation in mice with an impaired skin barrier.
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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.