The role of AQP4 in neuromyelitis optica: More answers, more questions

被引：27

作者：

Yang, Xin ^{[1
,2
]}

Ransom, Bruce R. ^{[3
]}

Ma, Jian-Fang ^{[1
,2
]}

机构：

[1] Shanghai Jiao Tong Univ, Sch Med, Ruijin Hosp, Dept Neurol, Shanghai 200025, Peoples R China

[2] Shanghai Jiao Tong Univ, Sch Med, Ruijin Hosp, Inst Neurol, Shanghai 200025, Peoples R China

[3] Univ Washington, Sch Med, Dept Neurol, Seattle, WA 98039 USA

来源：

JOURNAL OF NEUROIMMUNOLOGY | 2016年 / 298卷

关键词：

Complement; Demyelination; Glutamate; Neuromyelitis optica; Potassium channel; Water channel protein aquaporin-4; MULTIPLE-SCLEROSIS; IN-VIVO; AQUAPORIN; 4; GLUTAMATE RECEPTORS; EXTRACELLULAR-SPACE; TRANSVERSE MYELITIS; GAP-JUNCTIONS; IGG BINDING; D-ASPARTATE; NMO-IGG;

D O I：

10.1016/j.jneuroim.2016.06.002

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Neuromyelitis optica (NMO) is a recurrent inflammatory disease that preferentially targets the optic nerves and spinal cord. The presence of antibodies to the water channel protein aquaporin-4 (AQP4), expressed almost exclusively in astrocytes in the central nervous system (CNS), is a reliable biomarker for NMO. These antibodies, NMO-IgG, may be responsible for the sequential cascade of immune events, including IgG/IgM deposition, infiltration of granulocytes and complement-mediated cytotoxicity (i.e. astrocyte loss) and demyelination. This review summarizes current thinking about the role of NMO-IgG in the pathogenesis of this condition. New insights were also generated along with important additional questions. (C) 2016 Elsevier B.V. All rights reserved.

引用

页码：63 / 70

页数：8

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