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白癜风的病因发病机制

Aetiopathogenesis of Vitiligo.

作者信息

Boniface Katia

机构信息

University of Bordeaux, CNRS, Immuno ConcEpT, UMR 5164, Bordeaux, France.

出版信息

Dermatol Pract Concept. 2023 Dec 1;13(4S2):e2023314S. doi: 10.5826/dpc.1304S2a314S.

Abstract

Vitiligo is a chronic auto-immune disease characterized by skin depigmentation due to the loss of melanocytes. The better understanding of the disease mechanisms is currently undergoing a significant dynamism, opening a new era in therapeutic development. The pathophysiology of vitiligo has attracted the attention of researchers for years and many advances have been made in clarifying the crosstalk between the cellular players involved in the development of vitiligo lesions. The understanding of the complex interactions between epidermal cells (i.e. melanocytes and keratinocytes), dermal fibroblasts, and immune cells, led to a better characterization of the signals leading to the loss of melanocytes. Recent advances highlighted the role resident T memory cells in the development and recurrence of lesions. This narrative review aims to give an overview of the mechanisms leading to melanocyte disappearance in vitiligo, with a focus on the intercellular interaction network involved in the activation of the local skin immune response.

摘要

白癜风是一种慢性自身免疫性疾病,其特征是由于黑素细胞丢失导致皮肤色素脱失。目前,对该疾病机制的深入理解正在经历重大变革,开启了治疗发展的新时代。白癜风的病理生理学多年来一直吸引着研究人员的关注,在阐明参与白癜风皮损发展的细胞间相互作用方面已经取得了许多进展。对表皮细胞(即黑素细胞和角质形成细胞)、真皮成纤维细胞和免疫细胞之间复杂相互作用的理解,使得导致黑素细胞丢失的信号得到了更好的表征。最近的进展突出了驻留T记忆细胞在皮损发展和复发中的作用。这篇叙述性综述旨在概述导致白癜风中黑素细胞消失的机制,重点关注参与局部皮肤免疫反应激活的细胞间相互作用网络。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b031/10824321/86fd75551894/dp1304S2a314Sg001.jpg

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