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Basis for the barrier abnormality in atopic dermatitis: outside-inside-outside pathogenic mechanisms.

Elias PM, Hatano Y, Williams ML

Dermatology Service, Veterans Affairs Medical Center, San Francisco, Calif 94121, USA. eliasp@derm.ucsf.edu

Until quite recently, the pathogenesis of atopic dermatitis (AD) has been attributed to primary abnormalities of the immune system. Intensive study revealed the key roles played by T(H)1/T(H)2 cell dysregulation, IgE production, mast cell hyperactivity, and dendritic cell signaling in the evolution of the chronic, pruritic, inflammatory dermatosis that characterizes AD. Accordingly, current therapy has been largely directed toward ameliorating T(H)2-mediated inflammation and pruritus. In this review we will assess emerging evidence that inflammation in AD results from inherited and acquired insults to the barrier and the therapeutic implications of this paradigm.

Published 9 June 2008 in J Allergy Clin Immunol, 121(6): 1337-43.
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