Title of article
Pathogenesis of Atopic Dermatitis: Current Paradigm
Author/Authors
Furue, Masutaka Research and Clinical Center for Yusho and Dioxin - Kyushu University Hospital - Fukuoka, Japan , Ulzii, Dugarmaa Kyushu University Hospital - Fukuoka, Japan , Vu, Yen Hai Kyushu University Hospital - Fukuoka, Japan , Tsuji, Gaku Kyushu University Hospital - Fukuoka, Japan , Kido-Nakahara, Makiko Kyushu University Hospital - Fukuoka, Japan , Nakahara, Takeshi Kyushu University Hospital - Fukuoka, Japan
Pages
11
From page
97
To page
107
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
OX40 , IL-31 , IL-13 , IL-4 , Atopic Dermatitis
Journal title
Astroparticle Physics
Serial Year
2019
Record number
2487335
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