Development of axonal degeneration by passive transfer of antiganglioside antibody and therapeutic trial for it.

我们先前报道了GD1b神经节苷脂致敏的兔感觉性共济失调神经病(SAN)的发生。为探讨抗GD1b抗体在发病机制中的作用，我们将病兔抗GD1b抗血清注入正常兔体内。其病理改变与GD1b诱导的SAN相同，提示抗GD1b抗体是格林-巴利综合征(GBS)动物模型的重要致病因素，抗GD1b抗体与深感觉障碍和脱髓鞘形式有关。GD1b定位于大的初级感觉神经元和结旁髓鞘。单特异性抗GD1b抗体可能与这些区域结合，引起上述临床特征。肺炎支原体感染后GBS患者的急性期血清中存在抗Gal-C抗体。我们发现在肺炎支原体中存在一个类似Gal-C的结构，这表明主要的髓鞘糖脂Gal-C和肺炎支原体之间存在分子模拟。

We previously reported the development of sensory ataxic neuropathy (SAN) in rabbits sensitized with GD 1b ganglioside. To investigate the pathogenetic role of anti-GD 1b antibody, we performed intravenous infusion of anti-GD 1b antiserum from the affected rabbits into normal rabbits. It produced axonal degeneration with macrophage infiltration in primary sensory neurons with central axons extending to the dorsal column, the same pathological findings for GD 1b-induced SAN, showing that anti-GD 1b antibody is an important pathogenetic factor in this animal model Guillain-Barre syndrome (GBS) with monospecific IgG anti-GD 1b antibody was associated with disturbance in deep sensation and demyelinating form. GD 1b is localized in large primary sensory neurons and paranodal myelin. Monospecific anti-GD 1b antibody may bind to those regions and cause the above clinical features. Anti-Gal-C antibodies are present in the acute-phase sera from GBS patients subsequent to M. pneumoniae. We showed that a Gal-C-like structure is present in M. pneumoniae, indicative of molecular mimicry between a major myelin glycolipid, Gal-C, and M. pneumoniae.