Immune Alterations in IgE and Non IgE-Associated Atopic Dermatitis
Giampaolo Ricci*, Elisabetta Calamelli, Francesca Cipriani
Identifiers and Pagination:Year: 2014
First Page: 60
Last Page: 67
Publisher Id: TODJ-8-60
Article History:Received Date: 10/07/2014
Revision Received Date: 29/09/2014
Acceptance Date: 30/09/2014
Electronic publication date: 06/12/2014
Collection year: 2014
open-access license: This is an open access article distributed under the terms of the Creative Commons Attribution 4.0 International Public License (CC-BY 4.0), a copy of which is available at: https://creativecommons.org/licenses/by/4.0/legalcode. This license permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Atopic dermatitis is a complex disease in which a strong interaction between alterations of skin barrier and the adaptive immune system coexists. In the recent years, new findings have underlined the importance of skin proteins, especially filaggrin, which participate to the outmost layers of the skin. To strengthen this physical barrier, many factors are available, such as antimicrobial peptides, chemokines and cytokines produced by keratinocytes. Skin disruption can easily allow the allergen penetration and the local keratinocytes can promote the adaptive immune response toward a Th2 phenotype. On the other side, allergic Th2 cytokines may downregulate the production of skin barrier proteins, facilitating the penetration of allergens. Moreover, data on murine models show the absolute relevance of the systemic immune system to develop clinical skin reaction. Since the clinical aspect of patients with AD does not show different patterns whatever is the prevalent underlying mechanism, in clinical practice it is difficult to translate the different endotypes beside the IgE and non IgE associated forms. The aim of this review is to point out to the most recent knowledge in this field, which makes AD more difficult to frame in a unique clinical entity.