The immunological basis for treatment of stiff person syndrome

被引：26

作者：

Holmoy, Trygve ^{[1
,2
]}

Geis, Christian ^{[3
]}

机构：

[1] Univ Oslo, Ulleval Hosp, Dept Neurol, N-0407 Oslo, Norway

[2] Univ Oslo, Inst Immunol, N-0407 Oslo, Norway

[3] Univ Wurzburg, Dept Neurol, D-8700 Wurzburg, Germany

来源：

JOURNAL OF NEUROIMMUNOLOGY | 2011年 / 231卷 / 1-2期

关键词：

Stiff person syndrome; Aurtoantibodies; T cells; Autoimmunity; GLUTAMIC-ACID DECARBOXYLASE; CEREBELLAR GABAERGIC TRANSMISSION; T-CELLS; CEREBROSPINAL-FLUID; PROGRESSIVE ENCEPHALOMYELITIS; NEUROLOGICAL SYNDROMES; MULTIPLE-SCLEROSIS; AMPHIPHYSIN I; C-TERMINUS; AUTOANTIBODIES;

D O I：

10.1016/j.jneuroim.2010.09.014

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Antibodies against autoantigens involved in GABAergic neurotransmission are a shared feature of the different subtypes of stiff person syndrome (SPS). The autoantigens can be either presynaptic such as the smaller isoform of glutamic acid decarboxylase (GAD65), postsynaptic such as GABA-A receptor-associated protein and gephyrin, or located at the pre- and postsynaptic side such as amphiphysin. Most of these autoantigens are intracellular, and antibodies against GAD65 also occur in diabetes mellitus type 1 as well as other neurological diseases. Their pathogenic role has therefore been questioned. We here discuss the role of autoantibodies and T cells in SPS. (C) 2010 Elsevier B.V. All rights reserved.

引用

页码：55 / 60

页数：6

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