| Literature DB >> 28057434 |
Masutaka Furue1, Takahito Chiba2, Gaku Tsuji3, Dugarmaa Ulzii2, Makiko Kido-Nakahara2, Takeshi Nakahara4, Takafumi Kadono5.
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.Entities:
Keywords: Atopic dermatitis; Filaggrin; IgE autoreactivity; Th2; Th22
Mesh：
Substances：
Year: 2017 PMID： 28057434 DOI： 10.1016/j.alit.2016.12.002
Source DB: PubMed Journal: Allergol Int ISSN： 1323-8930 Impact factor: 5.836