Dermatitis Research Today is a free monthly online journal that collates and summarizes the latest research about Dermatitis, including details on contact-, seborrheic-, atopic-, allergic-dermatitis, treatment.

"Outside-to-inside" (and now back to "outside") pathogenic mechanisms in atopic dermatitis.

Elias PM, Steinhoff M

Dermatology Service, Veterans Affairs Medical Center, and Department of Dermatology, University of California, San Francisco, California 94121, USA. eliasp@derm.ucsf.edu

The pathogenesis of atopic dermatitis (AD) has been attributed largely to abnormalities in the adaptive immune system, with key roles played by T-helper 1(Th1)/Th2 cell dysregulation, IgE production, dendritic cell signaling, and mast-cell hyperactivity, resulting in the pruritic, inflammatory dermatosis that characterizes AD (Leung et al., 2004). Accordingly, therapy has been focused on ameliorating Th2-mediated inflammation and pruritus (eg, Leung, 2000). Indeed, there is emerging evidence that inflammation in AD results first from inherited and acquired insults that converge to alter epidermal structure and function, followed by immune system activation, which in turn has negative consequences for skin-barrier homeostasis. This cycle comprises an "outside-inside-outside" model of AD pathogenesis (Elias et al., in press).

Published 14 April 2008 in J Invest Dermatol, 128(5): 1067-70.
Full-text of this article is available online (may require subscription).

© 2004-2008 Dermatitis Research Today. All Rights Reserved.