Academic Neurosurgery Unit, St, George's, University of London, London, UK.
Acta Neuropathol Commun. 2014 Mar 31;2:35. doi: 10.1186/2051-5960-2-35.
Antibodies against myelin oligodendrocyte glycoprotein (MOG-IgG) are present in some neuromyelitis optica patients who lack antibodies against aquaporin-4 (AQP4-IgG). The effects of neuromyelitis optica MOG-IgG in the central nervous system have not been investigated in vivo. We microinjected MOG-IgG, obtained from patients with neuromyelitis optica, into mouse brains and compared the results with AQP4-IgG.
MOG-IgG caused myelin changes and altered the expression of axonal proteins that are essential for action potential firing, but did not produce inflammation, axonal loss, neuronal or astrocyte death. These changes were independent of complement and recovered within two weeks. By contrast, AQP4-IgG produced complement-mediated myelin loss, neuronal and astrocyte death with limited recovery at two weeks.
These differences mirror the better outcomes for MOG-IgG compared with AQP4-IgG patients and raise the possibility that MOG-IgG contributes to pathology in some neuromyelitis optica patients.
髓鞘少突胶质细胞糖蛋白（MOG-IgG）抗体存在于一些缺乏水通道蛋白-4（AQP4-IgG）抗体的视神经脊髓炎患者中。视神经脊髓炎 MOG-IgG 在中枢神经系统中的作用尚未在体内进行研究。我们将从视神经脊髓炎患者中获得的 MOG-IgG 微注射到小鼠大脑中，并将结果与 AQP4-IgG 进行比较。
MOG-IgG 导致髓鞘改变，并改变了对动作电位产生至关重要的轴突蛋白的表达，但没有引起炎症、轴突丢失、神经元或星形胶质细胞死亡。这些变化不依赖于补体，并且在两周内恢复。相比之下，AQP4-IgG 产生补体介导的髓鞘丢失、神经元和星形胶质细胞死亡，两周时恢复有限。
这些差异反映了 MOG-IgG 患者比 AQP4-IgG 患者的预后更好，并提出了 MOG-IgG 可能在一些视神经脊髓炎患者的病理中起作用的可能性。
