Atopic Dermatitis and Type 2 Immune Deviation

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

Research output: Contribution to journalReview articlepeer-review

Abstract

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.

Original languageEnglish
Pages (from-to)200-210
Number of pages11
JournalCurrent Treatment Options in Allergy
Volume6
Issue number3
DOIs
Publication statusPublished - Sep 2019

All Science Journal Classification (ASJC) codes

  • Immunology and Allergy
  • Medicine (miscellaneous)

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