Center for Fundamental Immunology, Benaroya Research Institute at Virginia Mason, Seattle, Washington; Department of Immunology, University of Washington School of Medicine, Seattle, Washington.
Ann Allergy Asthma Immunol. 2021 Sep;127(3):306-311. doi: 10.1016/j.anai.2021.06.004. Epub 2021 Jun 19.
Atopic dermatitis often precedes the development of other atopic diseases, and the atopic march describes this temporal relationship in the natural history of these diseases. Although the pathophysiological mechanisms that underlie this relationship are poorly understood, epidemiologic and genetic data have suggested that the skin might be an important route of sensitization to allergens.
Review of recent studies on the role of skin barrier defects in systemic allergen sensitization.
Recent publications on the relationship between skin barrier defects and expression of epithelial cell-derived cytokines.
Animal models have begun to elucidate on how skin barrier defects can lead to systemic allergen sensitization. Emerging data now suggest that epithelial cell-derived cytokines, such as thymic stromal lymphopoietin, drive the progression from atopic dermatitis to asthma and food allergy. Skin barrier defects can lead to induction of epithelial cell-derived cytokines, which in turn leads to the initiation and maintenance of allergic inflammation and the atopic march.
Development of new biologic drug targeting type 2 cytokines provides novel therapeutic interventions for atopic dermatitis.
特应性皮炎常先于其他特应性疾病发生，特应性进程描述了这些疾病自然史中的这种时间关系。尽管这种关系背后的病理生理机制尚不清楚，但流行病学和遗传学数据表明，皮肤可能是过敏原全身致敏的重要途径。
对皮肤屏障缺陷在全身过敏原致敏中作用的最新研究的综述。
关于皮肤屏障缺陷与上皮细胞衍生细胞因子表达之间关系的最新出版物。
动物模型已开始阐明皮肤屏障缺陷如何导致全身过敏原致敏。新出现的数据表明，上皮细胞衍生的细胞因子，如胸腺基质淋巴细胞生成素，推动了特应性皮炎向哮喘和食物过敏的发展。皮肤屏障缺陷可导致上皮细胞衍生细胞因子的诱导，进而导致过敏炎症的启动和维持以及特应性进程。
针对 2 型细胞因子的新型生物药物的开发为特应性皮炎提供了新的治疗干预措施。
