Kristensson K
Acta Neuropathol. 1976 Dec 21;36(4):307-14. doi: 10.1007/BF00699636.
In order to elucidate the role of humoral antibodies in the pathogenesis of myelin lesions in experimental allergic encephalomyelitis (EAE) a combined in vivo and in vitro study was done using rabbits immunized with the purified A1 basic protein. Rabbits injected with whole white matter were used for comparison. Demyelinating activity appeared in the rabbit sera 5 days after injection, as tested in myelinated organotypic tissue cultures. In spite of this no lesions of the myelin preceded the appearance of inflammatory cells in the living animals. In the spinal cord changes in vascular permeability, as revealed by leakage of Evans blue-albumin complex, appeared at the same time as the cells. In contrast to in vitro, the mere presence of circulating antibodies in vivo does not appear to be enough to cause structural changes of the myelin. Possible reasons for this discrepancy are discussed; it is emphasized that the inflammatory changes develope first in areas where the so-called blood-brain barrier to diffusion of proteins is lacking.
为了阐明体液抗体在实验性变应性脑脊髓炎(EAE)髓鞘病变发病机制中的作用,我们使用纯化的A1碱性蛋白免疫的兔子进行了一项体内和体外相结合的研究。注射全白质的兔子用作对照。在髓鞘化器官型组织培养中检测发现,注射后5天兔血清中出现脱髓鞘活性。尽管如此,在活体动物中,在炎性细胞出现之前,髓鞘并无病变。在脊髓中,伊文思蓝-白蛋白复合物渗漏显示的血管通透性变化与细胞出现的时间相同。与体外情况相反,体内循环抗体的单纯存在似乎不足以引起髓鞘的结构变化。文中讨论了这种差异的可能原因;强调炎性变化首先发生在缺乏所谓蛋白质扩散血脑屏障的区域。