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HERO ID
3985286
Reference Type
Journal Article
Subtype
Review
Title
Atopic dermatitis: immune deviation, barrier dysfunction, IgE autoreactivity and new therapies
Author(s)
Furue, M; Chiba, T; Tsuji, G; Ulzii, D; Kido-Nakahara, M; Nakahara, T; Kadono, T
Year
2017
Is Peer Reviewed?
Yes
Journal
Allergology International
ISSN:
1323-8930
EISSN:
1440-1592
Volume
66
Issue
3
Page Numbers
398-403
Language
English
PMID
28057434
DOI
10.1016/j.alit.2016.12.002
Web of Science Id
WOS:000405763000006
Abstract
Atopic dermatitis (AD) is a chronic or chronically relapsing, eczematous, severely pruritic skin disorder mostly associated with IgE elevation and skin barrier dysfunction due to decreased filaggrin expression. The lesional skin of AD exhibits Th2- and Th22-deviated immune reactions that are progressive during disease chronicity. Th2 and Th22 cytokines further deteriorate the skin barrier by inhibiting filaggrin expression. Some IgEs are reactive to self-antigens. The IgE autoreactivity may precipitate the chronicity of AD. Upon activation of the ORAI1 calcium channel, atopic epidermis releases large amounts of thymic stromal lymphopoietin (TSLP), which initiates the Th2 and Th22 immune response. Th2-derived interleukin-31 and TSLP induce an itch sensation. Taken together, TSLP/Th2/Th22 pathway is a promising target for developing new therapeutics for AD. Enhancing filaggrin expression using ligands for the aryl hydrocarbon receptor may also be an adjunctive measure to restore the disrupted barrier function specifically for AD.
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