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原标题：Tmem79突变小鼠皮肤屏障功能失调导致IL-17A依赖性的自发性皮肤和肺部炎症
背景：特应性皮炎（AD）与皮肤屏障调节失调有关，可能会诱发继发性过敏性疾病，例如哮喘。此前有报道称Tmem79ma/ma小鼠在编码跨膜蛋白79（或Mattrin）的基因中存在一个与AD有关的突变。由于Tmem79基因突变，这些小鼠的皮肤屏障存在缺陷，并可发展为自发性皮肤炎症。在这项研究中，评估了Tmem79ma/ma小鼠在自发性皮肤和肺部炎症发展中的潜在免疫反应。
方法：分析Tmem79ma/ma小鼠自发性皮肤和肺部炎症的发生。我们进一步调查了皮肤金黄色葡萄球菌感染的易感性。
将Tmem79ma/ma与IL-17A缺陷型小鼠杂交，以探讨IL-17A对自发性皮肤和肺部疾病的影响。
结果：Tmem79ma/ma小鼠发生IL-17A依赖性自发性AD样炎症，并且对金黄色葡萄球菌感染不敏感。突变小鼠在皮炎发生后发展为气道炎症。从皮肤疾病到肺部疾病的发展取决于适应性免疫，Th17和TCRγδT细胞的皮肤扩张促进了这种疾病的发展。
结论：缺乏Tmem79/Mattrin表达的小鼠皮肤屏障有缺陷。这些小鼠成年后发展为皮炎，并继发肺部炎症。皮肤和肺部炎症的发展是IL-17A依赖性的，并由TCRγδ T细胞介导。


延伸阅读
Allergy                                                    
Dysregulated skin barrier function in Tmem79 mutant mice promotes IL-17A-dependent spontaneous skin and lung inflammation
DOI: 10.1111/all.14488
Abstract:
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
First Author:
Sean P. Saunders
Correspondence:
Padraic Fallon, School of Medicine, Trinity College Dublin, Dublin 2, Ireland.
All Authors:
Sean P. Saunders, Achilleas Floudas, Tara Moran, Ciara M. Byrne, Michael D. Rooney, Caoimhe M. R. Fahy, Joan A. Geoghegan, Yoichiro Iwakura, Padraic G. Fallon, Christian Schwartz
2020-12-11 Article 
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