Epicutaneous sensitization and asthma

Abstract

Pediatric asthma preceded by eczema is associated with genetic mutation in skin-barrier related molecule, filaggrin, suggesting that disruption of skin barrier is related with the development of asthma. Skin barrier function, constituted of filaggrin and extracellular lipids in the stratum corneum and tight junction in the stratum granulosum, can be disrupted not only by genetic abnormality, but also by many mechanical, chemical, and biological factors. Allergen sensitization through the impaired skin induces the expression of specific molecules such as thymic stromal lymphopoietin and interleukin-23. These molecules exacerbate type 2-immune responses essential for the development of asthma and other allergic diseases. In contrast, epicutaneous allergen immunotherapy, in which low dose antigen is applied on the normal skin, induces regulatory T cells, and possibly suppresses the progression of allergic march. Further studies to clarify the mechanisms and immunological responses of epicutaneous allergen sensitization would lead to novel therapeutics for the prevention of early-onset allergic asthma.