Health & Environmental Research Online (HERO)


Print Feedback Export to File
3985286 
Journal Article 
Review 
Atopic dermatitis: immune deviation, barrier dysfunction, IgE autoreactivity and new therapies 
Furue, M; Chiba, T; Tsuji, G; Ulzii, D; Kido-Nakahara, M; Nakahara, T; Kadono, T 
2017 
Yes 
Allergology International
ISSN: 1323-8930
EISSN: 1440-1592 
66 
3 
398-403 
English 
28057434 
WOS:000405763000006 
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. 
• PCBs
     Targeted review search
          Source