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

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

Research output: Contribution to journalReview article

38 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)398-403
Number of pages6
JournalAllergology International
Volume66
Issue number3
DOIs
Publication statusPublished - Jul 1 2017

Fingerprint

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

Cite this

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

In: Allergology International, Vol. 66, No. 3, 01.07.2017, p. 398-403.

Research output: Contribution to journalReview article

@article{ebc017f7208e492a9739e7c46e8f2b84,
title = "Atopic dermatitis: immune deviation, barrier dysfunction, IgE autoreactivity and new therapies",
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.",
author = "Masutaka Furue and Takahito Chiba and Gaku Tsuji and Dugarmaa Ulzii and Makiko Nakahara and Takeshi Nakahara and Takafumi Kadono",
year = "2017",
month = "7",
day = "1",
doi = "10.1016/j.alit.2016.12.002",
language = "English",
volume = "66",
pages = "398--403",
journal = "Allergology International",
issn = "1323-8930",
publisher = "Japanese Society of Allergology",
number = "3",

}

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 - Nakahara, Makiko

AU - Nakahara, Takeshi

AU - Kadono, Takafumi

PY - 2017/7/1

Y1 - 2017/7/1

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.

UR - http://www.scopus.com/inward/record.url?scp=85008334911&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85008334911&partnerID=8YFLogxK

U2 - 10.1016/j.alit.2016.12.002

DO - 10.1016/j.alit.2016.12.002

M3 - Review article

C2 - 28057434

AN - SCOPUS:85008334911

VL - 66

SP - 398

EP - 403

JO - Allergology International

JF - Allergology International

SN - 1323-8930

IS - 3

ER -