Current Allergy and Asthma Reports

, Volume 8, Issue 4, pp 299–305

Skin barrier function


DOI: 10.1007/s11882-008-0048-0

Cite this article as:
Elias, P.M. Curr Allergy Asthma Rep (2008) 8: 299. doi:10.1007/s11882-008-0048-0


Like other inflammatory dermatoses, the pathogenesis of atopic dermatitis (AD) has been largely attributed to abnormalities in adaptive immunity. T helper (Th) cell types 1 and 2 cell dysregulation, IgE production, mast cell hyperactivity, and dendritic cell signaling are thought to account for the chronic, pruritic, and inflammatory dermatosis that characterizes AD. Not surprisingly, therapy has been directed toward ameliorating Th2-mediated inflammation and pruritus. Here, we review emerging evidence that inflammation in AD occurs downstream to inherited and acquired insults to the barrier. Therapy based upon this new view of pathogenesis should emphasize approaches that correct the primary abnormality in barrier function, which drives downstream inflammation and allows unrestricted antigen access.

Copyright information

© Springer Science+Business Media, LLC 2008

Authors and Affiliations

  1. 1.Dermatology Service (190)VA Medical CenterSan FranciscoUSA

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