Scholarlink

<p>Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by loss of immune tolerance, systemic inflammation, autoantibody production, and immune complex formation. Neuropsychiatric systemic lupus erythematosus (NPSLE) represents one of the most severe manifestations of the disease and may involve both the central and peripheral nervous systems. Its pathogenesis remains incompletely understood and reflects the interplay among systemic immune dysregulation, vascular injury, blood-brain and blood-CSF barrier dysfunction, and local neuroinflammatory processes.</p><p><?noindent??>Current evidence supports two partially overlapping pathogenic pathways: an autoimmune-inflammatory and a thrombo-ischemic pathway. These mechanisms promote disruption of the blood-brain barrier, infiltration of immune cells into the central nervous system, activation of microglia, and neuronal dysfunction. Increasing evidence also highlights the role of neutrophil extracellular traps, complement activation, type I interferon signaling, and autoreactive lymphocytes in driving neuroinflammation.</p><p><?noindent??>The heterogeneity of clinical manifestations and the diversity of underlying mechanisms make NPSLE a major diagnostic and therapeutic challenge. This review summarizes current knowledge on the immunopathogenesis of NPSLE, with particular attention to the strength of evidence supporting individual mechanisms. Human clinical studies provide important associative data, whereas animal models and cell-based systems offer mechanistic insight into selected pathways. We also discuss emerging biomarkers, limitations of current evidence, and potential therapeutic targets that may improve future diagnosis, stratification, and management of NPSLE.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Immunopathogenesis of neuropsychiatric systemic lupus erythematosus: current insights into inflammatory and thrombotic pathways

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年6月23日

查看全文
  • Igor Adamski,
  • Anna Wardowska

摘要

Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by loss of immune tolerance, systemic inflammation, autoantibody production, and immune complex formation. Neuropsychiatric systemic lupus erythematosus (NPSLE) represents one of the most severe manifestations of the disease and may involve both the central and peripheral nervous systems. Its pathogenesis remains incompletely understood and reflects the interplay among systemic immune dysregulation, vascular injury, blood-brain and blood-CSF barrier dysfunction, and local neuroinflammatory processes.

Current evidence supports two partially overlapping pathogenic pathways: an autoimmune-inflammatory and a thrombo-ischemic pathway. These mechanisms promote disruption of the blood-brain barrier, infiltration of immune cells into the central nervous system, activation of microglia, and neuronal dysfunction. Increasing evidence also highlights the role of neutrophil extracellular traps, complement activation, type I interferon signaling, and autoreactive lymphocytes in driving neuroinflammation.

The heterogeneity of clinical manifestations and the diversity of underlying mechanisms make NPSLE a major diagnostic and therapeutic challenge. This review summarizes current knowledge on the immunopathogenesis of NPSLE, with particular attention to the strength of evidence supporting individual mechanisms. Human clinical studies provide important associative data, whereas animal models and cell-based systems offer mechanistic insight into selected pathways. We also discuss emerging biomarkers, limitations of current evidence, and potential therapeutic targets that may improve future diagnosis, stratification, and management of NPSLE.