Atopic Dermatitis and Type 2 Immune Deviation

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

研究成果: ジャーナルへの寄稿総説査読

2 被引用数 (Scopus)


Purpose of the review: To summarize recent topics on type 2 signatures in atopic dermatitis (AD). Recent findings: Therapeutic success of anti-IL-4 receptor antibody dupilumab does suggest that type 2 cytokines IL-4 and IL-13 have pivotal roles in the pathogenesis of AD. Lesional skin of AD expresses increased levels of IL-4 and IL-13. In parallel, type 2 chemokines such as CCL17, CCL22, and CCL26 are overexpressed in AD, and these chemokines recruit type 2 T cells and eosinophils. IL-4 and IL-13 downregulate the expression of filaggrin and exacerbate epidermal barrier dysfunction. Keratinocytes in barrier-disrupted epidermis produce thymic stromal lymphopoietin, IL-25 and IL-33, which enhance the type 2 immune response. IL-31, released from type 2 T cells, is an essential pruritogenic cytokine. IL-4 and IL-13 amplify the IL-31-mediated neuronal signal. Summary: Type 2 cytokines IL-4 and IL-13 are profoundly associated with three cardinal features of AD: barrier dysfunction, skin inflammation, and chronic pruritus. These findings explain the high efficacy of dupilumab in the treatment of AD.

ジャーナルCurrent Treatment Options in Allergy
出版ステータス出版済み - 9月 2019

!!!All Science Journal Classification (ASJC) codes

  • 免疫アレルギー学
  • 医学(その他)


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