Han Hongwei, Roan Florence, Ziegler Steven F
Immunology Program, Benaroya Research Institute, Seattle, WA, USA.
Department of Immunology, University of Washington School of Medicine, Seattle, WA, USA.
Immunol Rev. 2017 Jul;278(1):116-130. doi: 10.1111/imr.12546.
Atopic dermatitis often precedes the development of other atopic diseases. The atopic march describes this temporal relationship in the natural history of atopic diseases. Although the pathophysiological mechanisms that underlie this relationship are poorly understood, epidemiological and genetic data have suggested that the skin might be an important route of sensitization to allergens. Animal models have begun to elucidate how skin barrier defects can lead to systemic allergen sensitization. Emerging data now suggest that epithelial cell-derived cytokines such as thymic stromal lymphopoietin (TSLP), IL-33, and IL-25 may drive the progression from atopic dermatitis to asthma and food allergy. This review focuses on current concepts of the role of skin barrier defects and epithelial cell-derived cytokines in the initiation and maintenance of allergic inflammation and the atopic march.
特应性皮炎常先于其他特应性疾病出现。特应性进程描述了特应性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，皮肤可能是对变应原致敏的重要途径。动物模型已开始阐明皮肤屏障缺陷如何导致全身性变应原致敏。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（TSLP）、白细胞介素-33（IL-33）和白细胞介素-25（IL-25）可能推动从特应性皮炎向哮喘和食物过敏的进展。本综述重点关注皮肤屏障缺陷和上皮细胞衍生的细胞因子在过敏性炎症的起始和维持以及特应性进程中的作用的当前概念。
