特应性皮炎的发病机制

近年来关于特应性皮炎（AD）的发病机制研究进展迅速，目前研究认为AD发病主要是皮肤屏障功能障碍、免疫应答异常和环境因素刺激共同作用的结果。遗传学研究证实，皮肤屏障功能相关基因和免疫应答及其调控基因参与AD发病。皮肤屏障功能障碍是皮肤激发和维持AD炎症的重要原因。在皮肤屏障受损的基础上，外源过敏原和微生物就很容易透过角质层进入表皮和真皮，进而引发免疫应答。AD瘙痒的病理生理学机制还不清楚，除外组胺，其他的炎症介质和致痒原等也参与介导了瘙痒发生。

Pathogenisis of Atopic Dermatitis

The research on the pathogenesis of atopic dermatitis has been the focus of many researchers, and has gained great progress recently. Now it has been accepted that skin barrier dysfunction, aberrant immune response and environmental stimulator are the three main contributors to the pathogenesis of AD. Genetic studies have proved that skin barrier related genes and immune responses and its regulating genes participate in the pathogenesis of AD. Skin barrier dysfunction is the reason of the initiation and maintenance of AD inflammation. The mechanism for the itch of AD is not clear yet. Besides histamine, other inflammatory reagents and pruritogens participate in the itch.