دورية أكاديمية

IL-1β induces thymic stromal lymphopoietin and an atopic dermatitis-like phenotype in reconstructed healthy human epidermis

التفاصيل البيبلوغرافية
العنوان: IL-1β induces thymic stromal lymphopoietin and an atopic dermatitis-like phenotype in reconstructed healthy human epidermis
المؤلفون: Bernard, Marine, Carrasco, Cédric, Laoubi, Léo, Guiraud, Béatrice, Rozières, Aurore, Goujon, Catherine, Duplan, Hélène, Bessou-Touya, Sandrine, Nicolas, Jean-François, Vocanson, Marc, Galliano, Marie-Florence
المساهمون: Immunologie de l'allergie cutanée et vaccination – Immunology of skin allergy and vaccination, Centre International de Recherche en Infectiologie (CIRI), École normale supérieure de Lyon (ENS de Lyon)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Université Jean Monnet - Saint-Étienne (UJM)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-École normale supérieure de Lyon (ENS de Lyon)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Université Jean Monnet - Saint-Étienne (UJM)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Service d'immunologie Centre Hospitalier Lyon Sud - HCL, Centre Hospitalier Lyon Sud CHU - HCL (CHLS), Hospices Civils de Lyon (HCL)-Hospices Civils de Lyon (HCL), Laboratoire de Pharmacochimie Pierre Fabre Dermo-Cosmétique, Centre de Recherche Pierre Fabre (Centre de R&D Pierre Fabre), PIERRE FABRE-PIERRE FABRE, Autophagie infection et immunité - Autophagy Infection Immunity (APY)
المصدر: The Journal of Pathology ; https://hal.science/hal-01911419Test ; The Journal of Pathology, 2017, 242 (2), pp.234-245. ⟨10.1002/path.4887⟩
بيانات النشر: HAL CCSD
سنة النشر: 2017
المجموعة: HAL Lyon 1 (University Claude Bernard Lyon 1)
مصطلحات موضوعية: Epidermis, Middle Aged, NF-kappa B, Phenotype, reconstructed human epidermis, TSLP, Young Adult, IL-1β, Humans, Homeostasis, filaggrin, Female, Intermediate Filament Proteins, Male, Interleukin-1beta, Interleukin 1 Receptor Antagonist Protein, Adult, Antibodies, Monoclonal, atopic dermatitis, Cell Differentiation, Cytokines, Dermatitis, Atopic, [SDV.IMM]Life Sciences [q-bio]/Immunology, [SDV.MP.BAC]Life Sciences [q-bio]/Microbiology and Parasitology/Bacteriology, [SDV.MP.VIR]Life Sciences [q-bio]/Microbiology and Parasitology/Virology
الوصف: International audience ; Atopic dermatitis (AD) is a common skin inflammatory disease characterized by the production of thymic stromal lymphopoietin (TSLP) and marked TH 2 polarization. Recent studies suggest that IL-1β contributes to the development of AD skin inflammation. Here, we have investigated the impact of IL-1β signalling on the epidermal homeostasis of both healthy subjects and AD patients [with functional filaggrin (FLG) alleles], with particular attention to TSLP production and keratinocyte differentiation. In healthy reconstructed human epidermis (RHE), IL-1β promoted (i) robust secretion of TSLP in an NF-\kappaB-dependent manner and (ii) a significant decrease in the expression of filaggrin and other proteins of the epidermal differentiation complex. These effects were prevented by treatment of RHE with the anti-IL-1β mAb canakinumab and by the IL-1 receptor antagonist anakinra. Interestingly, RHE generated from AD donors behaved like that of healthy individuals and showed comparable responses to IL-1β signals. Collectively, our results suggest that IL-1β may be an early key mediator for the acquisition of an AD phenotype through induction of TSLP and alteration of the epidermal homeostasis. Copyright \textcopyright 2017 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
نوع الوثيقة: article in journal/newspaper
اللغة: English
العلاقة: info:eu-repo/semantics/altIdentifier/pmid/28191908; hal-01911419; https://hal.science/hal-01911419Test; PUBMED: 28191908
DOI: 10.1002/path.4887
الإتاحة: https://doi.org/10.1002/path.4887Test
https://hal.science/hal-01911419Test
رقم الانضمام: edsbas.5438B5CC
قاعدة البيانات: BASE