脱髓鞘和星形胶质细胞病的发病机制：水通道蛋白 4、MOG、GFAP、GRP78 及其他自身抗体。
Pathomechanisms in demyelination and astrocytopathy: autoantibodies to AQP4, MOG, GFAP, GRP78 and beyond.
机构信息
Institute of Clinical Neuroimmunology, Biomedical Center and University Hospital, Ludwig-Maximilians-Universität München, Munich, Germany.
出版信息
Curr Opin Neurol. 2022 Jun 1;35(3):427-435. doi: 10.1097/WCO.0000000000001052.
PURPOSE OF REVIEW
The purpose of this review is to highlight the recently emerging pathomechanisms of diseases associated with autoantibodies to AQP4, MOG, GFAP, GRP78 and further novel targets. We discuss novel biomarkers and therapeutic approaches.
RECENT FINDINGS
Although complement-mediated cytotoxicity (CDC) is regarded as the major effector mechanism for AQP4-IgG in neuromyelitis optica spectrum disorders (NMOSD), recent studies helped to understand the relevance of complement-independent effector mechanisms. For MOG-IgG mediated diseases the role of CDC is less clear. MOG-IgG may trigger a tightly controlled FcR and BTK-driven microglia proliferative response in MOG-antibody-associated diseases. Differences of antibody-mediated tissue damage may reflect differential response to therapy. In addition, antibodies to GFAP, GRP78 and further novel targets have been implicated in demyelination and astrocytopathy.
SUMMARY
Elucidating the whole spectrum of effector functions in diseases mediated by AQP4-IgG and MOG-IgG and understanding the role of additional novel autoantibodies involved in demyelination and astrocytopathy may guide further novel treatment decisions.
目的综述
本文旨在强调与水通道蛋白 4（AQP4）、髓鞘少突胶质细胞糖蛋白（MOG）、胶质纤维酸性蛋白（GFAP）、葡萄糖调节蛋白 78（GRP78）和其他新靶点自身抗体相关疾病的新出现的病理机制。我们讨论了新的生物标志物和治疗方法。
最近发现
尽管补体介导的细胞毒性（CDC）被认为是视神经脊髓炎谱系疾病（NMOSD）中 AQP4-IgG 的主要效应机制，但最近的研究有助于了解补体非依赖性效应机制的相关性。对于 MOG-IgG 介导的疾病，CDC 的作用尚不清楚。MOG-IgG 可能在 MOG 抗体相关性疾病中触发紧密控制的 FcR 和 BTK 驱动的小胶质细胞增殖反应。抗体介导的组织损伤的差异可能反映出对治疗的不同反应。此外，GFAP、GRP78 和其他新靶点的抗体也与脱髓鞘和星形胶质细胞病变有关。
总结
阐明 AQP4-IgG 和 MOG-IgG 介导的疾病中所有的效应功能，并了解参与脱髓鞘和星形胶质细胞病变的其他新自身抗体的作用，可能有助于进一步的新型治疗决策。
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