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

我们之前报道过GD 1b神经节苷脂致敏兔的感觉性共济失调神经病（SAN）的发展。为了研究抗gd - 1b抗体的致病作用，我们将患病家兔的抗gd - 1b抗血清静脉滴注到正常家兔体内。GD - 1b诱导的SAN病理结果与此相同，表明抗GD - 1b抗体是该动物模型格林-巴利综合征（GBS）的重要致病因素，单特异性IgG抗GD - 1b抗体与深部感觉障碍和脱髓鞘形式相关。GD 1b定位于大的初级感觉神经元和副神经节髓鞘。单特异性抗gd 1b抗体可能与这些区域结合，导致上述临床特征。抗gal - c抗体存在于GBS患者肺炎支原体感染后的急性期血清中。我们发现，在肺炎支原体中存在Gal-C样结构，表明主要髓磷脂糖脂、Gal-C和肺炎支原体之间的分子相似性。

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.