Dysregulated skin barrier function in Tmem79 mutant mice promotes IL-17A-dependent spontaneous skin and lung inflammation
© 2020 The Authors. Allergy published by European Academy of Allergy and Clinical Immunology and John Wiley & Sons Ltd..
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. Tmem79ma/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, Tmem79ma/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 Tmem79ma/ma mice was analyzed. We further investigated susceptibility to cutaneous Staphylococcus aureus infection. Tmem79ma/ma were crossed to IL-17A-deficient mice to address the contribution of IL-17A to spontaneous skin and lung disease.
RESULTS: Tmem79ma/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.
| Medienart: |
E-Artikel |
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| Erscheinungsjahr: |
2020 |
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| Erschienen: |
2020 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:75 |
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| Enthalten in: |
Allergy - 75(2020), 12 vom: 15. Dez., Seite 3216-3227 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Saunders, Sean P [VerfasserIn] |
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| Links: |
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| Themen: |
Cutaneous inflammation |
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| Anmerkungen: |
Date Completed 14.05.2021 Date Revised 31.05.2022 published: Print-Electronic Citation Status MEDLINE |
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| doi: |
10.1111/all.14488 |
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| funding: |
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| Förderinstitution / Projekttitel: |
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| PPN (Katalog-ID): |
NLM312214642 |
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| 100 | 1 | |a Saunders, Sean P |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Dysregulated skin barrier function in Tmem79 mutant mice promotes IL-17A-dependent spontaneous skin and lung inflammation |
| 264 | 1 | |c 2020 | |
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| 500 | |a Date Completed 14.05.2021 | ||
| 500 | |a Date Revised 31.05.2022 | ||
| 500 | |a published: Print-Electronic | ||
| 500 | |a Citation Status MEDLINE | ||
| 520 | |a © 2020 The Authors. Allergy published by European Academy of Allergy and Clinical Immunology and John Wiley & Sons Ltd. | ||
| 520 | |a 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. Tmem79ma/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, Tmem79ma/ma mice were assessed for the underlying immunological response in the development of spontaneous skin and lung inflammation | ||
| 520 | |a METHODS: Development of spontaneous skin and lung inflammation in Tmem79ma/ma mice was analyzed. We further investigated susceptibility to cutaneous Staphylococcus aureus infection. Tmem79ma/ma were crossed to IL-17A-deficient mice to address the contribution of IL-17A to spontaneous skin and lung disease | ||
| 520 | |a RESULTS: Tmem79ma/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 | ||
| 520 | |a 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 | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a Research Support, Non-U.S. Gov't | |
| 650 | 4 | |a Tmem79 | |
| 650 | 4 | |a cutaneous inflammation | |
| 650 | 4 | |a interleukin-17A | |
| 650 | 4 | |a lung inflammation | |
| 650 | 4 | |a skin barrier | |
| 650 | 7 | |a Il17a protein, mouse |2 NLM | |
| 650 | 7 | |a Interleukin-17 |2 NLM | |
| 650 | 7 | |a Membrane Proteins |2 NLM | |
| 650 | 7 | |a Tmem79 protein, mouse |2 NLM | |
| 700 | 1 | |a Floudas, Achilleas |e verfasserin |4 aut | |
| 700 | 1 | |a Moran, Tara |e verfasserin |4 aut | |
| 700 | 1 | |a Byrne, Ciara M |e verfasserin |4 aut | |
| 700 | 1 | |a Rooney, Michael D |e verfasserin |4 aut | |
| 700 | 1 | |a Fahy, Caoimhe M R |e verfasserin |4 aut | |
| 700 | 1 | |a Geoghegan, Joan A |e verfasserin |4 aut | |
| 700 | 1 | |a Iwakura, Yoichiro |e verfasserin |4 aut | |
| 700 | 1 | |a Fallon, Padraic G |e verfasserin |4 aut | |
| 700 | 1 | |a Schwartz, Christian |e verfasserin |4 aut | |
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