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本文引用的文献

1
Disease amelioration with tocilizumab in a treatment-resistant patient with neuromyelitis optica: implication for cellular immune responses.托珠单抗治疗抵抗型视神经脊髓炎患者的疾病改善:对细胞免疫应答的影响。
JAMA Neurol. 2013 Mar 1;70(3):390-3. doi: 10.1001/jamaneurol.2013.668.
2
Cerebrospinal fluid interleukin-6 and glial fibrillary acidic protein levels are increased during initial neuromyelitis optica attacks.在视神经脊髓炎初始发作期间,脑脊液中白细胞介素-6 和神经胶质纤维酸性蛋白的水平升高。
Clin Chim Acta. 2013 Jun 5;421:181-3. doi: 10.1016/j.cca.2013.03.020. Epub 2013 Mar 25.
3
Distinct serum cytokine profiles in neuromyelitis optica and multiple sclerosis.视神经脊髓炎和多发性硬化症患者血清细胞因子谱的差异。
J Interferon Cytokine Res. 2013 Feb;33(2):58-64. doi: 10.1089/jir.2012.0040.
4
Interleukin 6 receptor blockade in patients with neuromyelitis optica nonresponsive to anti-CD20 therapy.白细胞介素 6 受体阻断剂治疗抗 CD20 治疗反应不佳的视神经脊髓炎患者。
JAMA Neurol. 2013 Mar 1;70(3):394-7. doi: 10.1001/jamaneurol.2013.1246.
5
Cerebrospinal fluid high-mobility group box protein 1 in neuromyelitis optica and multiple sclerosis.视神经脊髓炎和多发性硬化症中的脑脊液高迁移率族蛋白 1。
Neuroimmunomodulation. 2013;20(2):113-8. doi: 10.1159/000345994. Epub 2013 Jan 10.
6
CXCL13 is a biomarker of inflammation in multiple sclerosis, neuromyelitis optica, and other neurological conditions.CXCL13 是多发性硬化症、视神经脊髓炎和其他神经疾病炎症的生物标志物。
Mult Scler. 2013 Aug;19(9):1204-8. doi: 10.1177/1352458512473362. Epub 2013 Jan 15.
7
CSF high-mobility group box 1 is associated with intrathecal inflammation and astrocytic damage in neuromyelitis optica.脑脊液高迁移率族蛋白 B1 与视神经脊髓炎的鞘内炎症和星形胶质细胞损伤有关。
J Neurol Neurosurg Psychiatry. 2013 May;84(5):517-22. doi: 10.1136/jnnp-2012-304039. Epub 2012 Dec 19.
8
Increased plasma interleukin-32 expression in patients with neuromyelitis optica.视神经脊髓炎患者血浆白细胞介素-32 表达增加。
J Clin Immunol. 2013 Apr;33(3):666-70. doi: 10.1007/s10875-012-9837-2. Epub 2012 Nov 21.
9
Elevated plasma high-mobility group box 1 protein is a potential marker for neuromyelitis optica.血浆高迁移率族蛋白 1 水平升高可能是视神经脊髓炎的一个潜在标志物。
Neuroscience. 2012 Dec 13;226:510-6. doi: 10.1016/j.neuroscience.2012.08.041.
10
The ex vivo production of IL-6 and IL-21 by CD4+ T cells is directly associated with neurological disability in neuromyelitis optica patients.视神经脊髓炎患者 CD4+T 细胞体外产生的 IL-6 和 IL-21 与神经功能缺损直接相关。
J Clin Immunol. 2013 Jan;33(1):179-89. doi: 10.1007/s10875-012-9780-2. Epub 2012 Sep 5.

视神经脊髓炎中的细胞因子和趋化因子:发病机制和治疗意义。

Cytokines and chemokines in neuromyelitis optica: pathogenetic and therapeutic implications.

机构信息

Department of Neurology, Graduate School of Medicine, Chiba University, Chiba.

出版信息

Brain Pathol. 2014 Jan;24(1):67-73. doi: 10.1111/bpa.12097.

DOI:10.1111/bpa.12097
PMID:24345220
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8029308/
Abstract

Neuromyelitis optica (NMO) is characterized by severe optic neuritis and longitudinally extensive transverse myelitis. The discovery of an NMO-specific autoantibody to the aquaporin-4 (AQP4) water channel has improved knowledge of NMO pathogenesis. Many studies have focused on inflammatory and pathological biomarkers of NMO, including cytokines and chemokines. Increased concentrations of T helper (Th)17- and Th2-related cytokines and chemokines may be essential factors for developing NMO inflammatory lesions. For example, interleukin-6 could play important roles in NMO pathogenesis, as it is involved in the survival of plasmablasts that produce anti-AQP4 antibody in peripheral circulation and in the enhancement of inflammation in the central nervous system. Therefore, assessment of these useful biomarkers may become a supportive criterion for diagnosing NMO. Significant advances in the understanding of NMO pathogenesis will lead to the development of novel treatment strategies. This review focuses on the current advances in NMO immunological research, particularly that of cytokines and chemokines.

摘要

视神经脊髓炎(NMO)的特征是严重的视神经炎和长节段横贯性脊髓炎。水通道蛋白-4(AQP4)的 NMO 特异性自身抗体的发现提高了对 NMO 发病机制的认识。许多研究都集中在 NMO 的炎症和病理生物标志物上,包括细胞因子和趋化因子。Th17 和 Th2 相关细胞因子和趋化因子的浓度增加可能是发生 NMO 炎症病变的重要因素。例如,白细胞介素-6 可能在 NMO 的发病机制中发挥重要作用,因为它参与了外周循环中产生抗 AQP4 抗体的浆母细胞的存活,并增强了中枢神经系统的炎症。因此,这些有用的生物标志物的评估可能成为诊断 NMO 的支持标准。对 NMO 发病机制的理解的显著进展将导致新的治疗策略的发展。这篇综述重点介绍了 NMO 免疫学研究的最新进展,特别是细胞因子和趋化因子的研究进展。