Published online Feb 2, 2015. doi: 10.5314/wjd.v4.i1.16
Peer-review started: September 22, 2014
First decision: November 1, 2014
Revised: November 29, 2014
Accepted: December 16, 2014
Article in press: December 17, 2014
Published online: February 2, 2015
Core tip: Atopic diseases [including atopic dermatitis (AD), allergic rhinitis and asthma] are characterised by Th2-type inflammation. Research over the past decade has highlighted a crucial role for primary skin barrier impairment in the pathogenesis of AD and associated atopic phenotypes. Notably, the epidermal protein, filaggrin, epidermal serine proteases, and the pro-Th2 cytokine thymic stromal lymphopoietin, have been implicated in disease development. We review the evidence upholding a role for epidermal defects in the initiation of skin inflammation in AD, allergic sensitization and pathogenesis of the “atopic march”, and discuss the clinical implications of these findings.