Rheumatology Division, Lincoln Medical and Mental Health Center, 234 E. 149th Street, New York, NY 10451, USA.
Mod Rheumatol. 2009;19(5):457-68. doi: 10.1007/s10165-009-0198-5. Epub 2009 Jul 18.
Systemic lupus erythematosus is a chronic, multisystemic, autoimmune disease that may involve the central, peripheral, and autonomic nervous systems and can present with a wide variety of neurological and psychiatric manifestations. In this article, we review the recent literature pertaining to the pathogenesis of neuropsychiatric systemic lupus erythematosus (NPSLE). We searched the PUBMED database with no chronological constraints using the following terms: "neuropsychiatric systemic lupus erythematosus" cross-referenced with the terms "pathogenesis" and "biomarkers" for full-text articles in English. The etiology of NPSLE is as yet unknown, though numerous autoantibodies and cytokines have been suggested as possible mediators. Of the numerous autoantibodies and biomarkers examined, anti-phospholipid, anti-ribosomal P, anti-neuronal, anti-glial fibrillary acidic protein (GFAP), anti-endothelial cell, anti-N-methyl-D: -aspartate (NMDA), microtubule-associated protein 2 (MAP-2), and matrix metalloproteinase-9 (MMP-9) appear to be elevated in patients with NPSLE. Cytokines that may be involved in the pathology of NPSLE include interleukin (IL)-2, IL-6, IL-8, IL-10, tumor necrosis factor (TNF)-alpha, and interferons (IFN)-alpha and -gamma. With continued advances in immunological research, new insights into the pathophysiologic mechanisms of NPSLE may lead to the development of biomarkers and new treatment strategies.
系统性红斑狼疮是一种慢性、多系统自身免疫性疾病，可能累及中枢、周围和自主神经系统，并可表现出多种神经和精神表现。本文综述了神经精神性系统性红斑狼疮（NPSLE）发病机制的最新文献。我们在 PUBMED 数据库中以英文全文形式，无时间限制地使用以下术语进行检索：“神经精神性系统性红斑狼疮”与“发病机制”和“生物标志物”交叉引用。NPSLE 的病因尚不清楚，尽管有许多自身抗体和细胞因子被认为是可能的介质。在检查的众多自身抗体和生物标志物中，抗磷脂、抗核糖体 P、抗神经元、抗神经胶质纤维酸性蛋白（GFAP）、抗内皮细胞、抗 N-甲基-D：-天冬氨酸（NMDA）、微管相关蛋白 2（MAP-2）和基质金属蛋白酶-9（MMP-9）似乎在 NPSLE 患者中升高。可能参与 NPSLE 病理学的细胞因子包括白细胞介素（IL）-2、IL-6、IL-8、IL-10、肿瘤坏死因子（TNF）-α和干扰素（IFN）-α和 -γ。随着免疫研究的不断进展，对 NPSLE 病理生理机制的新认识可能会导致生物标志物和新治疗策略的发展。
