The IL-13–OVOL1–FLG axis in atopic dermatitis

Kazuhisa Furue, Takamichi Ito, Gaku Tsuji, Dugarmaa Ulzii, Yen Hai Vu, Makiko Kido-Nakahara, Takeshi Nakahara, Masutaka Furue

研究成果: ジャーナルへの寄稿評論記事

抄録

Despite sharing interleukin-4 receptor α (IL-4Rα) in their signaling cascades, IL-4 and IL-13 have different functions in atopic inflammation. IL-13 preferentially participates in the peripheral tissues because tissue-resident group 2 innate lymphoid cells produce IL-13 but not IL-4. In contrast, lymph node T follicular helper cells express IL-4 but not IL-13 to regulate B-cell immunity. The dominant microenvironment of IL-13 is evident in the lesional skin of atopic dermatitis (AD). The IL-13-rich local milieu causes barrier dysfunction by down-regulating the OVOL1–filaggrin (FLG) axis and up-regulating the periostin–IL-24 axis. Genome-wide association studies also point to the crucial involvement of the IL-13, OVOL1 and FLG genes in the pathogenesis of AD. Biologics targeting IL-13, such as the anti-IL-4Rα antibody dupilumab and the anti-IL-13 antibody tralokinumab, successfully improve AD lesions and further highlight the importance of IL-13 in the pathogenesis of AD.

元の言語英語
ページ(範囲)281-286
ページ数6
ジャーナルImmunology
158
発行部数4
DOI
出版物ステータス出版済み - 12 1 2019

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Interleukin-13
Atopic Dermatitis
Interleukin-4 Receptors
Interleukin-4
Genome-Wide Association Study
Helper-Inducer T-Lymphocytes
Biological Products
Anti-Idiotypic Antibodies
Immunity
B-Lymphocytes
Lymph Nodes
Lymphocytes
Inflammation
Skin

All Science Journal Classification (ASJC) codes

  • Immunology and Allergy
  • Immunology

これを引用

The IL-13–OVOL1–FLG axis in atopic dermatitis. / Furue, Kazuhisa; Ito, Takamichi; Tsuji, Gaku; Ulzii, Dugarmaa; Vu, Yen Hai; Kido-Nakahara, Makiko; Nakahara, Takeshi; Furue, Masutaka.

:: Immunology, 巻 158, 番号 4, 01.12.2019, p. 281-286.

研究成果: ジャーナルへの寄稿評論記事

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title = "The IL-13–OVOL1–FLG axis in atopic dermatitis",
abstract = "Despite sharing interleukin-4 receptor α (IL-4Rα) in their signaling cascades, IL-4 and IL-13 have different functions in atopic inflammation. IL-13 preferentially participates in the peripheral tissues because tissue-resident group 2 innate lymphoid cells produce IL-13 but not IL-4. In contrast, lymph node T follicular helper cells express IL-4 but not IL-13 to regulate B-cell immunity. The dominant microenvironment of IL-13 is evident in the lesional skin of atopic dermatitis (AD). The IL-13-rich local milieu causes barrier dysfunction by down-regulating the OVOL1–filaggrin (FLG) axis and up-regulating the periostin–IL-24 axis. Genome-wide association studies also point to the crucial involvement of the IL-13, OVOL1 and FLG genes in the pathogenesis of AD. Biologics targeting IL-13, such as the anti-IL-4Rα antibody dupilumab and the anti-IL-13 antibody tralokinumab, successfully improve AD lesions and further highlight the importance of IL-13 in the pathogenesis of AD.",
author = "Kazuhisa Furue and Takamichi Ito and Gaku Tsuji and Dugarmaa Ulzii and Vu, {Yen Hai} and Makiko Kido-Nakahara and Takeshi Nakahara and Masutaka Furue",
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AU - Furue, Kazuhisa

AU - Ito, Takamichi

AU - Tsuji, Gaku

AU - Ulzii, Dugarmaa

AU - Vu, Yen Hai

AU - Kido-Nakahara, Makiko

AU - Nakahara, Takeshi

AU - Furue, Masutaka

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N2 - Despite sharing interleukin-4 receptor α (IL-4Rα) in their signaling cascades, IL-4 and IL-13 have different functions in atopic inflammation. IL-13 preferentially participates in the peripheral tissues because tissue-resident group 2 innate lymphoid cells produce IL-13 but not IL-4. In contrast, lymph node T follicular helper cells express IL-4 but not IL-13 to regulate B-cell immunity. The dominant microenvironment of IL-13 is evident in the lesional skin of atopic dermatitis (AD). The IL-13-rich local milieu causes barrier dysfunction by down-regulating the OVOL1–filaggrin (FLG) axis and up-regulating the periostin–IL-24 axis. Genome-wide association studies also point to the crucial involvement of the IL-13, OVOL1 and FLG genes in the pathogenesis of AD. Biologics targeting IL-13, such as the anti-IL-4Rα antibody dupilumab and the anti-IL-13 antibody tralokinumab, successfully improve AD lesions and further highlight the importance of IL-13 in the pathogenesis of AD.

AB - Despite sharing interleukin-4 receptor α (IL-4Rα) in their signaling cascades, IL-4 and IL-13 have different functions in atopic inflammation. IL-13 preferentially participates in the peripheral tissues because tissue-resident group 2 innate lymphoid cells produce IL-13 but not IL-4. In contrast, lymph node T follicular helper cells express IL-4 but not IL-13 to regulate B-cell immunity. The dominant microenvironment of IL-13 is evident in the lesional skin of atopic dermatitis (AD). The IL-13-rich local milieu causes barrier dysfunction by down-regulating the OVOL1–filaggrin (FLG) axis and up-regulating the periostin–IL-24 axis. Genome-wide association studies also point to the crucial involvement of the IL-13, OVOL1 and FLG genes in the pathogenesis of AD. Biologics targeting IL-13, such as the anti-IL-4Rα antibody dupilumab and the anti-IL-13 antibody tralokinumab, successfully improve AD lesions and further highlight the importance of IL-13 in the pathogenesis of AD.

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