皮肤屏障功能障碍,特应性皮炎(AD)的定义特征,来自多个相互作用的系统。在AD中,皮肤炎症是由宿主-环境相互作用引起的,涉及角质形成细胞以及组织驻留的免疫细胞,如2型先天淋巴细胞,嗜碱性粒细胞,肥大细胞,和2型辅助性T细胞,产生2型细胞因子,包括IL-4、IL-5、IL-13和IL-31。2型炎症广泛影响屏障功能相关基因的表达,如细胞内结构蛋白,细胞外脂,和连接蛋白,并增强金黄色葡萄球菌的皮肤定植。全身性抗2型炎症疗法可能会改善AD患者功能失调的皮肤屏障。
Skin barrier dysfunction, a defining feature of atopic dermatitis (AD), arises from multiple interacting systems. In AD, skin inflammation is caused by host-environment interactions involving keratinocytes as well as tissue-resident immune cells such as type 2 innate lymphoid cells, basophils, mast cells, and T helper type 2 cells, which produce type 2 cytokines, including IL-4, IL-5, IL-13, and IL-31. Type 2 inflammation broadly impacts the expression of genes relevant for barrier function, such as intracellular structural proteins, extracellular lipids, and junctional proteins, and enhances Staphylococcus aureus skin colonization. Systemic anti‒type 2 inflammation therapies may improve dysfunctional skin barrier in AD.