Yoshimura T, Kunishita T, Sakai K, Endoh M, Namikawa T, Tabira T
J Neurol Sci. 1985 May-Jun;69(1-2):47-58. doi: 10.1016/0022-510x(85)90006-1.
A chronic experimental allergic encephalomyelitis (EAE) was produced in Hartley guinea pigs with bovine white matter proteolipid protein (PLP), in which the levels of myelin basic protein (MBP) and galactocerebroside (GC) were less than 0.014% and 0.13%, respectively, by our method of purification. Cells of an MBP-specific T-cell line did not proliferate in the presence of 100 micrograms of PLP and antigen-presenting cells. Eleven animals were sensitized with 250 micrograms of PLP in Freund's complete adjuvant. Three guinea pigs developed paraplegia about 45 days after sensitization. Histological examination of the three animals revealed marked demyelinating lesions in the spinal cord, particularly in the dorsal columns and subpial regions of the lateral and anterior columns. Another guinea pig without apparent clinical symptoms had demyelinating plaques in the dorsal columns of the spinal cord and periventricular white matter of the brain. Antibodies to PLP were highly elevated in the animals with demyelinating plaques but antibodies to MBP and GC were not elevated in the serum samples. Skin response to PLP was positive in sensitized animals, but was not related to the clinical state. Since none of four strain 13 guinea pigs developed chronic EAE, it seems to be strain specific. These results suggest that PLP is encephalitogenic and produces demyelination in the central nervous system without contamination by MBP or GC in Hartley guinea pigs.
用牛白质蛋白脂蛋白(PLP)在哈特利豚鼠中诱发慢性实验性变应性脑脊髓炎(EAE),通过我们的纯化方法,其中髓鞘碱性蛋白(MBP)和半乳糖脑苷脂(GC)的含量分别低于0.014%和0.13%。MBP特异性T细胞系的细胞在存在100微克PLP和抗原呈递细胞的情况下不增殖。11只动物用250微克PLP在弗氏完全佐剂中致敏。3只豚鼠在致敏后约45天出现截瘫。对这3只动物的组织学检查显示脊髓有明显的脱髓鞘病变,特别是在背柱以及外侧柱和前柱的软膜下区域。另一只没有明显临床症状的豚鼠在脊髓背柱和脑室周围白质有脱髓鞘斑块。有脱髓鞘斑块的动物中PLP抗体高度升高,但血清样本中MBP和GC抗体未升高。致敏动物对PLP的皮肤反应呈阳性,但与临床状态无关。由于13号品系的4只豚鼠均未发生慢性EAE,似乎具有品系特异性。这些结果表明,在哈特利豚鼠中,PLP具有致脑炎作用,并在中枢神经系统中产生脱髓鞘,而不受MBP或GC的污染。