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首页> 外文期刊>The Journal of dermatology >Pathogenic implication of epidermal scratch injury in psoriasis and atopic dermatitis
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Pathogenic implication of epidermal scratch injury in psoriasis and atopic dermatitis

机译:牛皮癣和特应性皮炎中表皮刮伤损伤的致病意义

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摘要

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 alpha 2, 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.
机译:机械性抓挠是一种影响皮肤的常见外部应力,由各种原因引起,如瘙痒。表皮角质形成细胞划痕损伤可在体外上调趋化因子(C-C基序)配体20(CCL20)的产生和释放,该配体选择性地吸引产生白细胞介素(IL)-17A的免疫细胞,这些细胞表达趋化因子(C-C基序)受体6(CCR6)。在以IL-17A为主的银屑病中,划痕诱导的CCL20上调以及随后产生IL-17A的免疫细胞和CCR6(+)成熟树突状细胞的积聚可能触发银屑病病变的发展,这一过程被称为Koebner现象。在以IL-4/IL-13为主的特应性皮炎中,瘙痒和随后的抓挠是主要症状。划痕诱导角质形成细胞产生CCL20可能解释了为什么IL-17A水平在特应性皮炎中也升高。相比之下,机械抓挠可能通过上调IL-13受体α2的表达来负向调节IL-13信号,后者在角质形成细胞中充当IL-13的诱饵受体。在这篇综述中,我们总结了当前关于表皮划痕损伤在银屑病和特应性皮炎中的致病作用的报道。

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