髓鞘少突胶质细胞糖蛋白
视神经脊髓炎
自身抗体
多发性硬化
免疫学
抗体
表位
医学
少突胶质细胞
单克隆抗体
脱髓鞘病
自身免疫
自身免疫性疾病
髓鞘
自身免疫性脑炎
中枢神经系统
疾病
免疫球蛋白G
纳塔利祖玛
髓鞘相关糖蛋白
实验性自身免疫性脑脊髓炎
生物
病理
神经系统
单克隆
脱髓鞘病
神经退行性变
作者
Hoi Kiu Wong,Samantha Ho,Qian Yu,Katherine S. Given,Dorina Shqau,Selia Baier,Stephan Winklmeier,Heike Rübsamen,Arek Kendirli,Kathrin Schanda,Eva Oswald,Katharina Elisabeth Marianne Bräuer,Franziska S. Thaler,Lisa Ann Gerdes,Regina Feederle,Martin Kerschensteiner,Markus Reindl,Mohsen Khademi,Fredrik Piehl,Tomas Olsson
标识
DOI:10.1126/scitranslmed.ady0403
摘要
The identification of autoantibodies against aquaporin-4 (AQP4) and myelin oligodendrocyte glycoprotein (MOG) has been essential in distinguishing neuromyelitis optica spectrum disorder (NMOSD) and MOG antibody-associated disease (MOGAD) from classical multiple sclerosis (MS), with important implications for treatment. However, for several patients within this disease spectrum, the target of the autoimmune response remains unknown. Here, we describe the modulator of VRAC current 1 (MLC1), a membrane protein with extracellular epitopes enriched at astrocytic end feet, as an autoantigen. Serum MLC1 antibodies were verified with a cell-based assay, identifying four MLC1 immunoglobulin G (IgG)-positive patients among 297 patients with inflammatory autoimmune diseases of the central nervous system who were screened. All four MLC1 IgG-positive patients exhibited overlapping yet atypical clinical features of MS and NMOSD and tested negative for AQP4 and MOG antibodies. Moreover, treatment with a monoclonal MLC1 antibody induced astrocytopathy in mouse cerebellar slice cultures and in a rat encephalitis model. Thus, MLC1 antibodies identify a subset of patients with an NMOSD-like phenotype, underscoring their potential as a disease marker with pathogenic relevance.
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