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2024 年出现可导致系统性红斑狼疮的 UNC93B1 变体

IF 29.4 1区 医学 Q1 RHEUMATOLOGY
Nature Reviews Rheumatology Pub Date : 2024-11-18 DOI:10.1038/s41584-024-01192-8
George C. Tsokos
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引用次数: 0

摘要

在过去一年中，有四项研究报告了编码 Toll 样受体（TLR）伴侣蛋白 UNC93B1 的 UNC93B1 的十个变异。所有变异都增加了 TLR7 和 TLR8 的信号传导，并导致年轻人患上系统性红斑狼疮，这凸显了针对该疾病的 TLR7 和 TLR8 的治疗潜力。
本文章由计算机程序翻译，如有差异，请以英文原文为准。
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The emergence of SLE-causing UNC93B1 variants in 2024
During the past year, four studies have reported ten mutations in UNC93B1, which encodes the Toll-like receptor (TLR) chaperone protein UNC93B1. All variants increased TLR7 and TLR8 signalling and caused systemic lupus erythematosus in young individuals, and highlight the therapeutic potential of targeting TLR7 and TLR8 in this disease.
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来源期刊
Nature Reviews Rheumatology
Nature Reviews Rheumatology 医学-风湿病学
CiteScore
29.90
自引率
0.90%
发文量
137
审稿时长
6-12 weeks
期刊介绍： Nature Reviews Rheumatology is part of the Nature Reviews portfolio of journals. The journal scope covers the entire spectrum of rheumatology research. We ensure that our articles are accessible to the widest possible audience.
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