Pathogenic implication of epidermal scratch injury in psoriasis and atopic dermatitis |
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Authors: | Kazuhisa Furue Dugarmaa Ulzii Yuka Tanaka Takamichi Ito Gaku Tsuji Makiko Kido-Nakahara Takeshi Nakahara Masutaka Furue |
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Affiliation: | 1. Department of Dermatology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan;2. Department of Dermatology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan Research and Clinical Center for Yusho and Dioxin, Kyushu University Hospital, Fukuoka, Japan |
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Abstract: | Mechanical scratching, a common external stress affecting the skin, is induced by various causes, such as pruritus. Scratch injury to epidermal keratinocytes upregulates the production and release of chemokine (C-C motif) ligand 20 (CCL20) in vitro, which selectively chemoattracts interleukin (IL)-17A-producing immune cells that express chemokine (C-C motif) receptor 6 (CCR6). In IL-17A-dominant psoriasis, scratch-induced CCL20 upregulation and subsequent accumulation of IL-17A-producing immune cells and CCR6+ mature dendritic cells may trigger the development of psoriatic lesions, a process known as the Koebner phenomenon. In IL-4/IL-13-dominant atopic dermatitis, pruritus and subsequent scratching are the primary symptoms. Scratch-induced CCL20 production from keratinocytes may explain why IL-17A levels are also elevated in atopic dermatitis. In contrast, mechanical scratching is likely to negatively regulate IL-13 signaling by upregulating the expression of IL-13 receptor α2, which serves as a decoy receptor for IL-13 in keratinocytes. In this review, we summarize current reports on topics related to the pathogenic role of epidermal scratch injury in psoriasis and atopic dermatitis. |
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Keywords: | atopic dermatitis chemokine (C-C motif) ligand 20 interleukin-13 receptor α2 psoriasis scratch injury |
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