Pathogenesis of Atopic Dermatitis

Current Paradigm

Research output: Contribution to journalArticle

Abstract

Atopic dermatitis (AD) is characterized by skin inflammation, barrier dysfunction and chronic pruritus. In this review, recent advances in the pathogenesis of AD are summarized. Clinical efficacy of the anti-IL-4 receptor antibody dupilumab implies that type 2 cytokines IL-4 and IL-13 have pivotal roles in atopic inflammation. The expression of IL-4 and IL-13 as well as type 2 chemokines such as CCL17, CCL22 and CCL26 is increased in the lesional skin of AD. In addition, IL-4 and IL-13 down-regulate the expression of filaggrin in keratinocytes and exacerbate epidermal barrier dysfunction. Keratinocytes in barrier-disrupted epidermis produce large amounts of thymic stromal lymphopoietin, IL-25 and IL-33, conducing to type 2 immune deviation via OX40L/OX40 signaling. IL-31, produced by type 2 T cells, is a cardinal pruritogenic cytokine. IL-4 and IL-13 also amplify the IL-31-mediated sensory nerve signal. These molecules are particularly important targets for future drug development for AD.

Original languageEnglish
Pages (from-to)97-107
Number of pages11
JournalIranian journal of immunology : IJI
Volume16
Issue number2
DOIs
Publication statusPublished - Jun 1 2019

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Interleukin-13
Atopic Dermatitis
Interleukin-4
Keratinocytes
Interleukin-4 Receptors
Cytokines
Inflammation
Skin
Pruritus
Chemokines
Epidermis
Down-Regulation
T-Lymphocytes
Antibodies
Pharmaceutical Preparations

All Science Journal Classification (ASJC) codes

  • Immunology and Allergy
  • Immunology

Cite this

Pathogenesis of Atopic Dermatitis : Current Paradigm. / Furue, Masutaka; Ulzii, Dugarmaa; Vu, Yen Hai; Tsuji, Gaku; Nakahara, Makiko; Nakahara, Takeshi.

In: Iranian journal of immunology : IJI, Vol. 16, No. 2, 01.06.2019, p. 97-107.

Research output: Contribution to journalArticle

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