The concept of "atopic march" has been well appreciated both by physicians and by dermatologists; eczema (atopic dermatitis) often precedes the development of airway diseases such as asthma and allergic rhinitis in atopic subjects. However, the underlying mechanisms for atopic march are less elucidated. It has been conceived that genetic susceptibility to atopy determines the phenotype of allergic diseases progressive from the skin to the airways, but recent discovery of filaggrin gene mutations that disturb the barrier function of the skin in patients with asthma and eczema now suggests the crucial role of epicutaneous sensitization as a precursory event for the development of asthma. In the present review, we describe updated genetic and immunological evidences that suggest the relationship between skin barrier-related molecules and the pathology of asthma.
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