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银屑病中的沃罗诺夫环与炎症后色素减退的机制。

The Woronoff Ring in Psoriasis and the Mechanisms of Postinflammatory Hypopigmentation.

机构信息

Department of Dermatology and Allergy, University Hospital, Ludwig Maximilian University of Munich, D-80337 München, Germany.

出版信息

Acta Derm Venereol. 2020 Jan 30;100(3):adv00031. doi: 10.2340/00015555-3385.

Abstract

The Woronoff ring is a ring-like hypopigmentation zone around regressing psoriasis lesions. Although it was first described more than 100 years ago, its aetiology has remained a mystery. Recent insights into the pathogenesis of psoriasis can now explain the origin of the Woronoff ring. Psoriasis involves an HLA-class I-restricted autoimmune response of CD8+ T cells against melanocytes in the epidermis. The pathogenic CD8+ T cells are not cytotoxic, but are characterized by the production of interleukin-17, interleukin-22 and tumour necrosis factor-α. Interleukin-17 and tumour necrosis factor-α act synergistically on melanocytes by increasing proliferation while inhibiting melanogenesis. This reduces the cellular melanin content despite an increased number of melanocytes in psoriatic lesions. As a consequence, during healing the prior influence of interleukin-17 and tumour necrosis factor-α, despite the increased density of melanocytes, leaves a hypopigmented zone at the edge of regressing psoriasis lesions, which becomes visible as the Woronoff ring. This mechanism can explain a long-discussed puzzling phenomenon in dermatology.

摘要

沃罗诺夫环是一种围绕着退行性银屑病皮损的环状色素减退区。尽管它在 100 多年前就被首次描述过,但它的病因一直是个谜。最近对银屑病发病机制的深入了解现在可以解释沃罗诺夫环的起源。银屑病涉及表皮黑素细胞的 HLA 类 I 受限的 CD8+ T 细胞自身免疫反应。致病性 CD8+ T 细胞没有细胞毒性,但特征是产生白细胞介素-17、白细胞介素-22 和肿瘤坏死因子-α。白细胞介素-17 和肿瘤坏死因子-α 通过增加增殖同时抑制黑色素生成,对黑素细胞产生协同作用。这会降低细胞内黑色素含量,尽管银屑病皮损中有更多的黑素细胞。因此,在愈合过程中,尽管黑素细胞密度增加,但白细胞介素-17 和肿瘤坏死因子-α 的先前影响会在退行性银屑病皮损的边缘留下一个色素减退区,这就是沃罗诺夫环。这一机制可以解释皮肤科中一个长期存在的令人困惑的现象。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c4c/9128907/a02285100052/ActaDV-100-3-5648-g001.jpg

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