Iranian Journal of Immunology

Pathogenesis of Atopic Dermatitis: Current Paradigm

Document Type : Review Article

Authors

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

Department of Dermatology, Faculty of Medical Sciences, Kyushu University, Japan

https://doi.org/10.22034/iji.2019.80253
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.

Keywords

Atopic Dermatitis
IL-4
IL-13
IL-31
OX40
Iranian Journal of Immunology
Volume 16, Issue 2
Spring 2019
Pages 97-107

Article View 13,162
PDF Download 8,655

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