Thymic stromal lymphopoietin, skin barrier dysfunction, and the atopic march

Abstract

ObjectiveAtopic 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. Data SourcesReview of recent studies on the role of skin barrier defects in systemic allergen sensitization. Study SelectionsRecent publications on the relationship between skin barrier defects and expression of epithelial cell–derived cytokines. ResultsAnimal 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. ConclusionDevelopment of new biologic drug targeting type 2 cytokines provides novel therapeutic interventions for atopic dermatitis.