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[炎症性神经系统疾病中血脑屏障的破坏]

[Disruption of the blood-brain barrier in inflammatory neurological diseases].

作者信息

Shimizu Fumitaka, Kanda Takashi

机构信息

Department of Neurology and Clinical Neuroscience, Yamaguchi University Graduate School of Medicine, Japan.

出版信息

Brain Nerve. 2013 Feb;65(2):165-76.

Abstract

The blood-brain barrier (BBB) restricts the exchange of humoral factors and cells between the blood and brain and thus plays a crucial role in maintaining cerebral homeostasis. Disruption of the BBB has been considered the initial key step of the disease process in some inflammatory neurological diseases, including multiple sclerosis (MS), neuromyelitis optica (NMO), and neuropsychiatric systemic lupus erythematosus (NPSLE). In MS, the BBB may be impaired before the formation of demyelinating foci or T-cell infiltration around small vessels; however, once the BBB is disrupted, massive infiltration of T cells, augmented expression of adhesion molecules on the endothelial cell surface, and leakage of inflammatory cytokines and antibodies aggravate the MS lesions. Recently, the disease-specific and pathogenic autoantibody "anti-AQP4" was detected in the sera of NMO patients. Thus, the destruction of the BBB is an important step in the development of NMO because the circulating anti-AQP4 antibodies have to pass through the BBB to reach the astrocytic endfeet, where AQP4 is localized. Several studies have shown an association between anti-NR2 antibodies in the serum or cerebrospinal fluid of NPSLE patients and neuropsychological manifestations. These antibodies may be involved in the pathogenesis of NPSLE, and the leaky BBB that allows the intrusion of circulating anti-NR2 antibodies is considered to play a crucial role in the disease process. Although some medications, including glucocorticoids and type 1 interferons, are known to repair the integrity of the BBB in an additive manner, the development of a novel disease-specific therapy, which focuses on repairing the integrity of the BBB, is awaited.

摘要

血脑屏障(BBB)限制了血液与大脑之间体液因子和细胞的交换,因此在维持脑内稳态中起着关键作用。在包括多发性硬化症(MS)、视神经脊髓炎(NMO)和神经精神性系统性红斑狼疮(NPSLE)在内的一些炎性神经系统疾病中,血脑屏障的破坏被认为是疾病进程的初始关键步骤。在MS中,血脑屏障可能在脱髓鞘病灶形成或小血管周围T细胞浸润之前就已受损;然而,一旦血脑屏障被破坏,T细胞的大量浸润、内皮细胞表面黏附分子表达增加以及炎性细胞因子和抗体的渗漏会加重MS病变。最近,在NMO患者的血清中检测到了疾病特异性致病自身抗体“抗水通道蛋白4(anti-AQP4)”。因此,血脑屏障的破坏是NMO发病过程中的一个重要步骤,因为循环中的抗AQP4抗体必须穿过血脑屏障才能到达水通道蛋白4所在的星形胶质细胞终足。多项研究表明,NPSLE患者血清或脑脊液中的抗NR2抗体与神经心理表现之间存在关联。这些抗体可能参与了NPSLE的发病机制,而允许循环抗NR2抗体侵入的渗漏血脑屏障被认为在疾病进程中起关键作用。尽管包括糖皮质激素和1型干扰素在内的一些药物已知可协同修复血脑屏障的完整性,但人们仍期待开发一种专注于修复血脑屏障完整性的新型疾病特异性疗法。

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