دورية أكاديمية
Dysregulated skin barrier function in Tmem79 mutant mice promotes IL-17A-dependent spontaneous skin and lung inflammation.
العنوان: | Dysregulated skin barrier function in Tmem79 mutant mice promotes IL-17A-dependent spontaneous skin and lung inflammation. |
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المؤلفون: | Saunders SP; Trinity Biomedical Sciences Institute, School of Medicine, Trinity College Dublin, Dublin, Ireland., Floudas A; Trinity Biomedical Sciences Institute, School of Medicine, Trinity College Dublin, Dublin, Ireland., Moran T; Trinity Biomedical Sciences Institute, School of Medicine, Trinity College Dublin, Dublin, Ireland.; National Children's Research Centre, Our Lady's Children's Hospital, Crumlin, Dublin, Ireland., Byrne CM; Trinity Biomedical Sciences Institute, School of Medicine, Trinity College Dublin, Dublin, Ireland., Rooney MD; Trinity Biomedical Sciences Institute, School of Medicine, Trinity College Dublin, Dublin, Ireland., Fahy CMR; Trinity Biomedical Sciences Institute, School of Medicine, Trinity College Dublin, Dublin, Ireland.; Dermatology, Our Lady's Children's Hospital Crumlin, Dublin, Ireland., Geoghegan JA; Department of Microbiology, Moyne Institute of Preventive Medicine, School of Genetics and Microbiology, Trinity College Dublin, Dublin, Ireland., Iwakura Y; Research Institute for Biomedical Sciences, Tokyo University of Science, Yamazaki, Japan., Fallon PG; Trinity Biomedical Sciences Institute, School of Medicine, Trinity College Dublin, Dublin, Ireland.; National Children's Research Centre, Our Lady's Children's Hospital, Crumlin, Dublin, Ireland., Schwartz C; Trinity Biomedical Sciences Institute, School of Medicine, Trinity College Dublin, Dublin, Ireland.; Mikrobiologisches Institut - Klinische Mikrobiologie, Immunologie und Hygiene, Universitätsklinikum Erlangen and Friedrich-Alexander Universität (FAU) Erlangen-Nürnberg, Erlangen, Germany. |
المصدر: | Allergy [Allergy] 2020 Dec; Vol. 75 (12), pp. 3216-3227. Date of Electronic Publication: 2020 Jul 22. |
نوع المنشور: | Journal Article; Research Support, Non-U.S. Gov't |
اللغة: | English |
بيانات الدورية: | Publisher: Wiley-Blackwell Country of Publication: Denmark NLM ID: 7804028 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1398-9995 (Electronic) Linking ISSN: 01054538 NLM ISO Abbreviation: Allergy Subsets: MEDLINE |
أسماء مطبوعة: | Publication: Copenhagen : Wiley-Blackwell Original Publication: Copenhagen, Munksgaard. |
مواضيع طبية MeSH: | Dermatitis, Atopic*/genetics , Interleukin-17*/genetics , Pneumonia*/genetics, Animals ; Disease Models, Animal ; Membrane Proteins/genetics ; Mice ; Skin |
مستخلص: | Background: Atopic dermatitis (AD) is associated with a dysregulation of the skin barrier and may predispose to the development of secondary allergic conditions, such as asthma. Tmem79 ma/ma mice harbor a mutation in the gene encoding Transmembrane Protein 79 (or Mattrin), which has previously been associated with AD. As a result of the Tmem79 gene mutation, these mice have a defective skin barrier and develop spontaneous skin inflammation. In this study, Tmem79 ma/ma mice were assessed for the underlying immunological response in the development of spontaneous skin and lung inflammation. Methods: Development of spontaneous skin and lung inflammation in Tmem79 ma/ma mice was analyzed. We further investigated susceptibility to cutaneous Staphylococcus aureus infection. Tmem79 ma/ma were crossed to IL-17A-deficient mice to address the contribution of IL-17A to spontaneous skin and lung disease. Results: Tmem79 ma/ma mice developed IL-17A-dependent spontaneous AD-like inflammation and were refractory to S aureus infection. Mutant mice progressed to airway inflammation subsequent to the occurrence of dermatitis. The progression from skin to lung disease is dependent on adaptive immunity and is facilitated by cutaneous expansion of Th17 and TCRγδ T cells. Conclusion: Mice lacking Tmem79/Mattrin expression have a defective skin barrier. In adulthood, these mice develop dermatitis with secondary progression to lung inflammation. The development of skin and lung inflammation is IL-17A-dependent and mediated by TCRγδ T cells. (© 2020 The Authors. Allergy published by European Academy of Allergy and Clinical Immunology and John Wiley & Sons Ltd.) |
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معلومات مُعتمدة: | 092530/Z/10/Z United Kingdom WT_ Wellcome Trust |
فهرسة مساهمة: | Keywords: Tmem79; cutaneous inflammation; interleukin-17A; lung inflammation; skin barrier |
المشرفين على المادة: | 0 (Il17a protein, mouse) 0 (Interleukin-17) 0 (Membrane Proteins) 0 (Tmem79 protein, mouse) |
تواريخ الأحداث: | Date Created: 20200710 Date Completed: 20210514 Latest Revision: 20220531 |
رمز التحديث: | 20221213 |
DOI: | 10.1111/all.14488 |
PMID: | 32644214 |
قاعدة البيانات: | MEDLINE |
تدمد: | 1398-9995 |
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DOI: | 10.1111/all.14488 |