Saida K, Saida T, Pleasure D E, Nishitani H
J Neurol Sci. 1983 Dec;62(1-3):77-93. doi: 10.1016/0022-510x(83)90191-0.
Experimental allergic neuritis (EAN) was induced in 2 groups of inbred Lewis rats by sensitization with P2 protein and peripheral nervous system (PNS) myelin, both purified from bovine intradural roots. Light- and electronmicroscopic study of P2-induced EAN revealed demyelinative lesions in spinal ganglia and root nerves and less frequently in peripheral nerves and root entry zones. Both small and large myelinated fibers were demyelinated, contradictory to the reported selective binding of anti-P2 antibodies to myelin of large fibers. The early lesions were characterised by perivenular lymphocytic infiltration, and subsequent "dissolution" of myelin sheath was associated with invasive of phagocytic cells. The distribution of demyelinative lesions and patterns of demyelination resembled those of PNS myelin-induced EAN except that the disease was milder and dissolution of myelin and intramyelinic edema were more frequently found in P2-induced EAN. The abundance of demyelination in P2-induced EAN strikes contrast to the scarcity of myelin change in experimental allergic encephalomyelitis (EAE) induced by myelin basic protein immunization.
通过用从牛硬脊膜内神经根纯化的P2蛋白和外周神经系统(PNS)髓磷脂致敏,在两组近交系Lewis大鼠中诱发实验性变应性神经炎(EAN)。对P2诱导的EAN进行光镜和电镜研究发现,脊髓神经节和神经根神经出现脱髓鞘病变,外周神经和神经根进入区较少出现。大小有髓纤维均发生脱髓鞘,这与报道的抗P2抗体与大纤维髓磷脂的选择性结合相矛盾。早期病变的特征是血管周围淋巴细胞浸润,随后髓鞘的“溶解”与吞噬细胞的侵入有关。脱髓鞘病变的分布和脱髓鞘模式与PNS髓磷脂诱导的EAN相似,只是该疾病较轻,且在P2诱导的EAN中更常发现髓鞘溶解和髓鞘内水肿。P2诱导的EAN中脱髓鞘的大量存在与髓鞘碱性蛋白免疫诱导的实验性变应性脑脊髓炎(EAE)中髓鞘变化的稀少形成鲜明对比。