Chalk J B, McCombe P A, Smith R, Pender M P
Department of Medicine, University of Queensland, Royal Brisbane Hospital, Australia.
J Neurol Sci. 1994 May;123(1-2):154-61. doi: 10.1016/0022-510x(94)90218-6.
Proteolipid protein (PLP) is the major protein of central nervous system (CNS) myelin. In some species, intradermal inoculation with PLP and adjuvants causes experimental autoimmune encephalomyelitis (PLP-EAE) characterized by neurological signs of tail and limb weakness and by inflammation and demyelination in the CNS. A previous study found that inoculation of Lewis rats with 100 micrograms of PLP causes PLP-EAE with a low incidence of neurological signs and a highly variable clinical course. In the present study we assessed PLP-EAE produced by inoculation with 1000 micrograms of PLP per rat. Fifty-one of 59 (86%) Lewis rats developed neurological signs 8 to 20 days (mean = 12.0 +/- 2.0) after inoculation with 1000 micrograms of PLP. In such rats, mononuclear cell infiltrates were present in the brain and spinal cord while primary demyelination occurred mainly in the subpial regions of the spinal cord, especially in the dorsal root entry and ventral root exit zones. The histological findings were compared with those in acute EAE induced in the Lewis rat by inoculation with whole CNS tissue or with myelin basic protein: in PLP-EAE, in contrast to these other models, the disease was essentially restricted to the CNS. This form of EAE should be useful in future studies of the consequences of autoimmunity to PLP.
蛋白脂蛋白（PLP）是中枢神经系统（CNS）髓鞘的主要蛋白质。在某些物种中，皮内接种PLP和佐剂会引发实验性自身免疫性脑脊髓炎（PLP-EAE），其特征为尾巴和肢体无力的神经学体征以及CNS中的炎症和脱髓鞘。先前的一项研究发现，给Lewis大鼠接种100微克PLP会导致PLP-EAE，其神经学体征的发生率较低且临床病程高度可变。在本研究中，我们评估了每只大鼠接种1000微克PLP所产生的PLP-EAE。59只Lewis大鼠中有51只（86%）在接种1000微克PLP后8至20天（平均 = 12.0 +/- 2.0）出现神经学体征。在这些大鼠中，大脑和脊髓存在单核细胞浸润，而原发性脱髓鞘主要发生在脊髓的软膜下区域，尤其是在背根进入区和腹根穿出区。将组织学结果与通过接种全CNS组织或髓鞘碱性蛋白诱导Lewis大鼠发生的急性EAE的结果进行比较：与这些其他模型相比，在PLP-EAE中，疾病基本局限于CNS。这种形式的EAE在未来关于针对PLP的自身免疫后果的研究中应该会很有用。
