Investigation on the significance of the epitope formed by ganglioside and phospholipid in neuroimmunological diseases

抗神经节苷脂抗体是诊断自身免疫性神经病的有用标记物。它们可能也参与了致病机制。细胞膜中的神经节苷脂被磷脂包围。我们研究了针对神经节苷脂和磷脂混合物的血清抗体活性。用GM1与PA、PS、PI等磷脂混合抗原，可增强格林-巴利综合征(GBS)患者抗GM1抗体的反应性。在Miller Fisher综合征患者中，抗GQ1b抗体未见这种增强。加入SM后，这两种抗体的活性都降低了。在GBS、慢性炎症性脱髓鞘多神经根神经病和多灶性运动神经病等自身免疫性神经病中，加入磷脂PA、PS和PI不能增强抗GM1 IgM抗体的反应性，而加入SM则能降低抗GM1抗体的反应性。在自身免疫性神经病中，SM降低抗神经节苷脂抗体的反应性，这可能是为什么抗神经节苷脂抗体不会对神经系统造成普遍的损害，而只影响神经节苷脂密集定位的地方。在混合抗原中加入PA可增强抗GalNAc-GD1a抗体的结合活性。这与上文所述的抗GM1抗体的结果相似。这可能是因为这两种抗体都与空肠弯曲菌感染前的死亡有关。我们的结果提示，在考虑抗神经节苷脂抗体在发病机制中的作用时，应更加重视磷脂的作用。在自身免疫性神经病以外的神经免疫性疾病中，需要对血清抗体进行类似的研究。

Antiganglioside antibodies are useful diagnostic markers of autoimmune neuropathies. They may be involved in the pathogenetic mechanisms as well. Gangliosides in the cell membrare are surrounded by phospholipids. We investigated serum antibody activities against a mixture of a ganglioside and a phospholipid. The reactivities of the anti-GM1 IgG antibodies in Guillain-Barre syndrome(GBS) were enhanced by the use of a mixture antigen of GM1 and such a phospholipid as PA,PS and PI. Such an enhancement was not seen for the anti-GQ1b IgG antibodies in Miller Fisher syndrome. The reactivates of both of those antibodies were reduced by the addition of SM. The reactivities of the anti-GM1 IgM antibodies in autoimmune neuropathies such as GBS, chronic inflammatory demyelinating polyradiculoneuropathy, and multifocal motor neuropathy were not enhanced by the addition of such a phospholiid as PA,PS and PI to the antigen mixture, while those were reduced by the addition of SM. The effect of SM that decreases the reactivities of the antiganglioside antibodies in autoimmune neuropathies may be the reason why an antiganglioside antibody does not cause ubiquitous damage on the neurological system but affects only the place where the ganglioside is densely localized. The binding activities of the anti-GalNAc-GD1a IgG antibodies were enhanced by the addition of PA to die antigen mixture. This resembles the results on the anti-GM1 IgG antibodies as described above. This may be due to the fact that both of the antibodies are associated with die preceding Campylobacter jejuni infection. Our results suggest that we should pay more attention to the effect by the phospholipids when we consider the role of the antiganglioside antibodies in the pathogenetic mechanisms. Similar investigation is needed on the serum antibodies in the neuroimmunological diseases other than autoimmune neuropathies.