Suppr超能文献

皮肤型红斑狼疮光敏性的当前概念

Current concepts of photosensitivity in cutaneous lupus erythematosus.

作者信息

Klein Benjamin, Kunz Manfred

机构信息

Department of Dermatology, Venereology, and Allergology, University Hospital Leipzig, Leipzig, Germany.

出版信息

Front Med (Lausanne). 2022 Aug 25;9:939594. doi: 10.3389/fmed.2022.939594. eCollection 2022.

Abstract

Cutaneous lupus erythematosus (CLE) represents a complex autoimmune disease with a broad phenotypic spectrum ranging from acute to chronic destructive cutaneous lesions. Patients with CLE exhibit high photosensitivity and ultraviolet (UV) irradiation can lead to systemic flares in systemic lupus erythematosus. However, the exact mechanisms how UV irradiation enhances cutaneous inflammation in lupus are not fully understood. Recently, new molecular mechanisms of UV-driven immune responses in CLE were identified, offering potential therapeutic approaches. Especially the induction of type I interferons, central cytokines in lupus pathogenesis which are released by various skin cells, have become the focus of current research. In this review, we describe current pathogenic concepts of photosensitivity in lupus erythematosus, including UV-driven activation of intracellular nucleic acid sensors, cellular cytokine production and immune cell activation. Furthermore, we discuss activated pathways contributing to enhanced apoptosis as well as intracellular translocation of autoantigens thereby promoting CLE upon UV light exposure.

摘要

皮肤红斑狼疮(CLE)是一种复杂的自身免疫性疾病,具有广泛的表型谱,涵盖从急性到慢性破坏性皮肤病变。CLE患者表现出高度的光敏性,紫外线(UV)照射可导致系统性红斑狼疮的全身发作。然而,紫外线照射如何增强狼疮皮肤炎症的确切机制尚未完全明确。最近,在CLE中发现了紫外线驱动免疫反应的新分子机制,为潜在的治疗方法提供了依据。特别是I型干扰素的诱导,它是狼疮发病机制中的核心细胞因子,由各种皮肤细胞释放,已成为当前研究的焦点。在本综述中,我们描述了红斑狼疮光敏性的当前致病概念,包括紫外线驱动的细胞内核酸传感器激活、细胞因子产生和免疫细胞激活。此外,我们讨论了导致细胞凋亡增强以及自身抗原细胞内易位的激活途径,从而在紫外线照射后促进CLE。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c46/9452788/e3841ef783ca/fmed-09-939594-g001.jpg

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验