Jin Haoli, He Rui, Oyoshi Michiko, Geha Raif S
Division of Immunology, Department of Medicine, Children's Hospital, Department of Pediatrics, Harvard Medical School, Boston, Massachusetts 02115, USA.
J Invest Dermatol. 2009 Jan;129(1):31-40. doi: 10.1038/jid.2008.106.
Atopic dermatitis (AD) is characterized by allergic skin inflammation. A hallmark of AD is dry itchy skin due, at least in part, to defects in skin genes that are important for maintaining barrier function. The pathogenesis of AD remains incompletely understood. Since the description of the Nc/Nga mouse as a spontaneously occurring model of AD, a number of other mouse models of AD have been developed. They can be categorized into three groups: (1) models induced by epicutaneous application of sensitizers; (2) transgenic mice that either overexpress or lack selective molecules; (3) mice that spontaneously develop AD-like skin lesions. These models have resulted in a better understanding of the pathogenesis of AD. This review discusses these models and emphasizes the role of mechanical skin injury and skin barrier dysfunction in eliciting allergic skin inflammation.
特应性皮炎(AD)的特征是过敏性皮肤炎症。AD的一个标志是皮肤干燥瘙痒,这至少部分归因于对维持屏障功能很重要的皮肤基因缺陷。AD的发病机制仍未完全了解。自从将Nc/Nga小鼠描述为AD的自发模型以来,已经开发了许多其他AD小鼠模型。它们可分为三组:(1)通过表皮涂抹致敏剂诱导的模型;(2)过表达或缺乏选择性分子的转基因小鼠;(3)自发出现类AD皮肤病变的小鼠。这些模型使人们对AD的发病机制有了更好的理解。本综述讨论了这些模型,并强调了机械性皮肤损伤和皮肤屏障功能障碍在引发过敏性皮肤炎症中的作用。