视神经脊髓炎
医学
多发性硬化
补体系统
髓鞘少突胶质细胞糖蛋白
免疫学
光谱紊乱
脱髓鞘病
发病机制
抗体
精神科
实验性自身免疫性脑脊髓炎
作者
Christian W. Keller,Joseph A. Lopez,Eva‐Maria Wendel,Sudarshini Ramanathan,Catharina C. Groß,Luisa Klotz,Markus Reindl,Russell C. Dale,Heinz Wiendl,Kevin Rostásy,Fabienne Brilot,Jan D. Lünemann
摘要
Myelin oligodendrocyte glycoprotein (MOG)-antibody (Ab)-associated diseases (MOGADs) account for a substantial proportion of pediatric and adult patients who present with acquired demyelinating disorders. Its pathogenesis and optimal therapy are incompletely understood. We profiled systemic complement activation in adult and pediatric patients with MOGAD compared with patients with relapse-onset multiple sclerosis, patients with neuromyelitis optica spectrum disorder, and pediatric control and adult healthy donors. Proteins indicative of systemic classical and alternative complement activation were substantially increased in patients with MOGAD compared to control groups. Elevated levels were detected in both adult and pediatric cases and across all clinical syndromes. Complement inhibition should be explored for its therapeutic merit in patients with MOGAD. ANN NEUROL 2021;90:976-982.
科研通智能强力驱动
Strongly Powered by AbleSci AI