抗髓鞘少突胶质细胞糖蛋白抗体诱导实验性自身免疫性脑脊髓炎的抗体反应。

Antibody response in MOG(35-55) induced EAE.

机构信息

Department of Pathology and Immunology, University of Geneva, Geneva, Switzerland.

出版信息

J Neuroimmunol. 2011 Dec 15;240-241:28-33. doi: 10.1016/j.jneuroim.2011.09.005. Epub 2011 Oct 10.

DOI:10.1016/j.jneuroim.2011.09.005

PMID:21993076

Abstract

Neurological deficit in experimental autoimmune encephalomyelitis (EAE) and multiple sclerosis is widely considered to be a consequence of synergistic T and B cell responses to central nervous system (CNS) antigens. We show that mice immunized with encephalitogenic myelin oligodendrocyte glycoprotein (MOG(35-55)) peptide develop significant serum levels of anti-MOG antibodies in parallel with disease progression. Furthermore, EAE mice developed antibodies against DNA and RNA, a serological hallmark observed in autoimmune diseases such as systemic lupus erythematosus. The presence of anti-nucleic responsive B cells and antibodies during EAE may highlight a previously unappreciated mechanism in the pathogenesis of CNS autoimmunity.

摘要

实验性自身免疫性脑脊髓炎（EAE）和多发性硬化症中的神经功能缺损被广泛认为是 T 细胞和 B 细胞对中枢神经系统（CNS）抗原的协同反应的结果。我们表明，用致脑炎髓鞘少突胶质细胞糖蛋白（MOG（35-55））肽免疫的小鼠在疾病进展的同时会产生显著的抗 MOG 抗体的血清水平。此外，EAE 小鼠还产生了针对 DNA 和 RNA 的抗体，这是红斑狼疮等自身免疫性疾病中的一种血清学特征。EAE 期间出现的抗核酸反应性 B 细胞和抗体可能突出了中枢神经系统自身免疫发病机制中的一个以前未被认识到的机制。