豚鼠脱髓鞘机制。将致敏与致脑性髓磷脂碱性蛋白和非致脑性脑成分分开。

B F Driscoll, J Kira, M W Kies, E C Alvord
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引用次数: 15

摘要

实验变应性脑脊髓炎(EAE)伴脱髓鞘中枢神经系统(CNS)病变,可在全豚鼠CNS组织致敏的豚鼠中诱发,但在纯化髓鞘碱性蛋白(BP)致敏的豚鼠中不能诱发。这种慢性脱髓鞘性EAE可能是细胞介导的对脑源性BP的免疫反应和对其他非脑源性CNS抗原的单独反应的综合结果。我们在这里报道,脱髓鞘性EAE可以通过单独的致敏来诱导细胞介导的BP反应和非致脑性CNS抗原的第二次免疫反应来诱导。豚鼠BP和全鸡脑在不同部位致敏的动物出现中枢神经系统脱髓鞘病变。只对BP或鸡脑敏感的动物不会发生脱髓鞘。
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Mechanism of demyelination in the guinea pig. Separate sensitization with encephalitogenic myelin basic protein and nonencephalitogenic brain components.

Experimental allergic encephalomyelitis (EAE), accompanied by demyelinating central nervous system (CNS) lesions, can be induced in guinea pigs sensitized with whole guinea pig CNS tissue, but not in animals sensitized with purified myelin basic protein (BP). This type of chronic demyelinating EAE is presumably a result of a combination of a cell-mediated immune response to the encephalitogenic BP and a separate response to other nonencephalitogenic CNS antigens. We report here that demyelinating EAE can be induced when separate sensitizations are used to induce a cell-mediated response to BP and a second immune response to nonencephalitogenic CNS antigens. Animals sensitized in separate sites with guinea pig BP and whole chicken brain develop CNS demyelinating lesions. Animals sensitized only to BP or chicken brain do not develop demyelination.

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