©The Author(s) 2015. Published by Baishideng Publishing Group Inc. All rights reserved.
From the outside-in: Epidermal targeting as a paradigm for atopic disease therapy
Rachel MC Gillespie, Department of Life Sciences, Imperial College London, SW7 2AZ London, United Kingdom
Sara J Brown, Dermatology and Genetic Medicine, College of Medicine, Dentistry and Nursing, University of Dundee, James Arrott Drive, Ninewells Hospital and Medical School, DD1 9SY Dundee, United Kingdom
Author contributions: Gillespie RMC performed the literature review, drafted the article and created the figures; Brown SJ supervised the work, reviewed and revised the manuscript and figures, and provided the clinical images with patient/parental consent.
Supported by Wellcome Trust Intermediate Clinical Fellowship, No. 086398/Z/08/Z.
Conflict-of-interest: The authors declare that they have no competing interests.
Correspondence to: Sara J Brown, MD, Dermatology and Genetic Medicine, College of Medicine, Dentistry and Nursing, University of Dundee, James Arrott Drive, Ninewells Hospital and Medical School, DD1 9SYD undee, United Kingdom. s.j.brown@dundee.ac.uk
Telephone: +44-13-82381056 Fax: +44-13-82740359
Received: September 21, 2014
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
Processing time: 120 Days and 14 Hours
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
Processing time: 120 Days and 14 Hours
Core Tip
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.