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
收藏
页码：63 / 70
页数：8
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