Takeda S, Ikuta F, Nagai Y
Jpn J Exp Med. 1980 Dec;50(6):453-62.
The light microscopical examinations were performed on the peripheral nerve (PN) lesions in rabbits induced by bovine peripheral nerve (BPN) myelin and by its components. Morphology of the PN lesions induced by P2 protein-ganglioside complex were equivalent to those induced by PN myelin (original EAN); and some of them were more remarkable in severity than the original EAN. The lesions were composed of myelin destruction, numerous macrophages containing myelin debris, completely demyelinated axons and remyelinating fibers. P2-I, acid treated P2-I and P2-II proteins induced PN lesions. Histologically they were moderate to minimal in severity in that order. However, when each protein was injected as the complex with ganglioside, PN lesions obviously became severer, respectively. These findings indicate the possibility that the P2-ganglioside complex may be involved in the chemical principle of EAN, and also the findings strongly support the theory proposed by Nagai et al. that gangliosides may play an essential role in rabbit EAN to give P2 protein a special conformation necessary for antigenic activity.
对牛周围神经（BPN）髓磷脂及其成分诱导的兔周围神经（PN）病变进行了光学显微镜检查。P2蛋白 - 神经节苷脂复合物诱导的PN病变形态与PN髓磷脂诱导的病变（原始实验性变态反应性神经炎，EAN）相当；其中一些病变的严重程度比原始EAN更显著。病变由髓磷脂破坏、大量含有髓磷脂碎片的巨噬细胞、完全脱髓鞘的轴突和再髓鞘化纤维组成。P2 - I、经酸处理的P2 - I和P2 - II蛋白诱导了PN病变。从组织学上看，它们的严重程度依次为中度到轻度。然而，当每种蛋白与神经节苷脂复合注射时，PN病变明显变得更严重。这些发现表明P2 - 神经节苷脂复合物可能参与了EAN的化学原理，并且这些发现有力地支持了Nagai等人提出的理论，即神经节苷脂可能在兔EAN中发挥重要作用，赋予P2蛋白抗原活性所需的特殊构象。
