TY - JOUR
T1 - Atopic dermatitis
T2 - immune deviation, barrier dysfunction, IgE autoreactivity and new therapies
AU - Furue, Masutaka
AU - Chiba, Takahito
AU - Tsuji, Gaku
AU - Ulzii, Dugarmaa
AU - Kido-Nakahara, Makiko
AU - Nakahara, Takeshi
AU - Kadono, Takafumi
N1 - Publisher Copyright:
© 2016 Japanese Society of Allergology
PY - 2017/7
Y1 - 2017/7
N2 - 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.
AB - 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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U2 - 10.1016/j.alit.2016.12.002
DO - 10.1016/j.alit.2016.12.002
M3 - Review article
C2 - 28057434
AN - SCOPUS:85008334911
SN - 1323-8930
VL - 66
SP - 398
EP - 403
JO - Allergology International
JF - Allergology International
IS - 3
ER -