Atopic dermatitis: immune deviation, barrier dysfunction, IgE autoreactivity and new therapies

Masutaka Furue, Takahito Chiba, Gaku Tsuji, Dugarmaa Ulzii, Makiko Kido-Nakahara, Takeshi Nakahara, Takafumi Kadono

研究成果: ジャーナルへの寄稿評論記事

46 引用 (Scopus)

抄録

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.

元の言語英語
ページ(範囲)398-403
ページ数6
ジャーナルAllergology International
66
発行部数3
DOI
出版物ステータス出版済み - 7 2017

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Atopic Dermatitis
Immunoglobulin E
Skin
Therapeutics
Aryl Hydrocarbon Receptors
Interleukins
Autoantigens
Calcium Channels
Epidermis
Cytokines
Ligands
thymic stromal lymphopoietin
filaggrin

All Science Journal Classification (ASJC) codes

  • Immunology and Allergy

これを引用

Atopic dermatitis : immune deviation, barrier dysfunction, IgE autoreactivity and new therapies. / Furue, Masutaka; Chiba, Takahito; Tsuji, Gaku; Ulzii, Dugarmaa; Kido-Nakahara, Makiko; Nakahara, Takeshi; Kadono, Takafumi.

:: Allergology International, 巻 66, 番号 3, 07.2017, p. 398-403.

研究成果: ジャーナルへの寄稿評論記事

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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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AU - Kido-Nakahara, Makiko

AU - Nakahara, Takeshi

AU - Kadono, Takafumi

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