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

OBJECTIVE

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.

DATA SOURCES

Review of recent studies on the role of skin barrier defects in systemic allergen sensitization.

STUDY SELECTIONS

Recent publications on the relationship between skin barrier defects and expression of epithelial cell-derived cytokines.

RESULTS

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.

CONCLUSION

Development of new biologic drug targeting type 2 cytokines provides novel therapeutic interventions for atopic dermatitis.