Abstract：
Atopic dermatitis is a skin disorder caused by skin dryness and barrier dysfunction, resulting in skin inflammation and chronic itch (or pruritus). The pathogenesis of atopic dermatitis is thought to be initiated by a lowering of the itch threshold due to dry skin. This lowering of the itch threshold is at least partially due to the increase in intraepidermal nerve fibers and sensitization of sensory nerves by interleukin (IL)-33 produced and secreted by keratinocytes. Such skin is easily prone to itch due to mechanical stimuli, such as rubbing of clothing and chemical stimuli from itch mediators. In patients with atopic dermatitis, once itch occurs, further itch is induced by scratching, and the associated scratching breaks down the skin barrier. Disruption of the skin barrier allows entry into the epidermis of external foreign substances, such as allergens derived from house dust mites, leading to an increased induction of type 2 inflammatory responses. As a result, type 2 cytokines IL-4, IL-13, and IL-31 are mainly secreted by Th2 cells, and their action on sensory nerve fibers causes further itch sensitization. These sequences of events are thought to occur simultaneously in patients with atopic dermatitis, leading to a vicious itch-scratch cycle. This vicious cycle becomes a negative spiral that leads to disease burden. Therefore, controlling itch is essential for the treatment of atopic dermatitis. In this review, we summarize and discuss advances in the mechanisms of peripheral itch sensitization in atopic dermatitis, focusing on skin barrier-neuro-immune triadic connectivity.
摘要：
特应性皮炎是由皮肤干燥和屏障功能障碍引起的皮肤病，导致皮肤炎症和慢性瘙痒（或瘙痒）。特应性皮炎的发病机理被认为是由皮肤干燥引起的瘙痒阈值降低引起的。瘙痒阈值的降低至少部分是由于表皮内神经纤维的增加和角质形成细胞产生和分泌的白介素(IL)-33对感觉神经的致敏。这种皮肤很容易因机械刺激而发痒，如摩擦衣服和瘙痒介质的化学刺激。在特应性皮炎患者中，一旦发痒,进一步的瘙痒是由抓挠引起的，和相关的抓挠打破了皮肤屏障。皮肤屏障的破坏允许外部异物进入表皮，如来自室内尘螨的过敏原，导致2型炎症反应的诱导增加。因此,2型细胞因子IL-4、IL-13和IL-31主要由Th2细胞分泌,它们对感觉神经纤维的作用会导致进一步的瘙痒敏化。这些事件序列被认为在特应性皮炎患者中同时发生，导致一个恶性的痒-抓循环。这种恶性循环成为导致疾病负担的负面螺旋。因此,控制瘙痒对治疗特应性皮炎至关重要。在这次审查中,我们总结并讨论了特应性皮炎外周瘙痒致敏机制的研究进展，专注于皮肤屏障-神经免疫三联连接。
