Antibodies as Mediators of Brain Pathology

被引:46
作者
Brimberg, Lior [1 ]
Mader, Simone [1 ]
Fujieda, Yuichiro [1 ]
Arinuma, Yoshiyuki [1 ]
Kowal, Czeslawa [1 ]
Volpe, Bruce T. [1 ]
Diamond, Betty [1 ]
机构
[1] Feinstein Inst Med Res, Manhasset, NY 11030 USA
关键词
SYSTEMIC-LUPUS-ERYTHEMATOSUS; AMPA RECEPTOR ANTIBODIES; STIFF-PERSON SYNDROME; NEUROMYELITIS-OPTICA; GLUTAMATE-RECEPTOR; LIMBIC ENCEPHALITIS; INTERFERON-BETA; COGNITIVE DYSFUNCTION; AQUAPORIN-4; ANTIBODY; DIAGNOSTIC-CRITERIA;
D O I
10.1016/j.it.2015.09.008
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The brain is normally sequestered from antibody exposure by the blood brain barrier. However, antibodies can access the brain during fetal development before the barrier achieves full integrity, and in disease states when barrier integrity is compromised. Recent studies suggest that antibodies contribute to brain pathology associated with autoimmune diseases such as systemic lupus erythematosus and neuromyelitis optica, and can lead to transient or permanent behavioral or cognitive abnormalities. We review these findings here and examine the circumstances associated with antibody entry into the brain, the routes of access and the mechanisms that then effect pathology. Understanding these processes and the nature and specificity of neuronal autoantibodies may reveal therapeutic strategies toward alleviating or preventing the neurological pathologies and behavioral abnormalities associated with autoimmune disease.
引用
收藏
页码:709 / 724
页数:16
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