Neuroimmune mechanisms of neuropsychiatric systemic lupus erythematosus

IF 5.8 2区医学 Q1 IMMUNOLOGY

Current Opinion in Immunology Pub Date : 2025-07-18 DOI:10.1016/j.coi.2025.102608

Stacie L Lin , Michael C Carroll

引用次数: 0

Abstract

In systemic lupus erythematosus (SLE), chronic autoimmunity and sustained inflammation can lead to the development of neuropsychiatric lupus (NPSLE) in up to 80% of patients. Elevated interferon-alpha (IFNα) is detected in serum and cerebrospinal fluid, making it a major focus in studies investigating the mediators of NPSLE. Others have emphasized the role of autoantibodies, such as anti-dsDNA, which have been shown to cross-react with neurotransmitter receptors and directly damage neurons. In this review, we present an integrative framework in which immune complexes deposited in the neurovasculature trigger local IFNα production in the brain. We discuss how complement activation amplifies inflammation by recruiting monocytes and promoting transcriptional shifts in glial cells toward reactive and neurotoxic states. Together, cellular and soluble immune effectors converge to disrupt neuronal function and drive the behavioral symptoms characteristic of NPSLE.

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神经精神系统性红斑狼疮的神经免疫机制

在系统性红斑狼疮（SLE）中，慢性自身免疫和持续炎症可导致高达80%的患者发展为神经精神性狼疮（NPSLE）。血清和脑脊液中检测到干扰素α (IFNα)升高，使其成为研究NPSLE介质的主要焦点。其他人强调自身抗体的作用，如抗dsdna，已被证明与神经递质受体交叉反应并直接损伤神经元。在这篇综述中，我们提出了一个综合框架，其中沉积在神经血管中的免疫复合物触发大脑中局部IFNα的产生。我们讨论了补体激活如何通过募集单核细胞和促进神经胶质细胞向反应性和神经毒性状态的转录转变来放大炎症。细胞和可溶性免疫效应物聚集在一起，破坏神经元功能并驱动NPSLE特征的行为症状。

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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来源期刊

Current Opinion in Immunology 医学-免疫学

CiteScore

13.30

自引率

1.40%

发文量

审稿时长

67 days

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