Immune responses against myelin basic protein and/or galactocerebroside cross-react with viruses: implications for demyelinating disease.
Immune responses against myelin basic protein and/or galactocerebroside cross-react with viruses: implications for demyelinating disease.
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针对髓磷脂碱性蛋白和/或半乳糖脑苷脂的免疫反应与病毒交叉反应：对脱髓鞘疾病的影响。
DOI：
10.1007/978-3-642-74594-2_8
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发表时间：
1989
影响因子：
--
通讯作者：
Fujinami,RS
中科院分区：
文献类型：
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作者：
Fujinami,RS
长期以来，人们一直推测病毒与其宿主自身组分共享交叉反应决定簇。直到最近才能通过使用单克隆抗体（Mab）和直接进行蛋白质序列比较来直接证明这一点。这种共享的共同决定子的概念是理解病毒诱导的自身免疫机制的基础。病毒感染后的脑脊髓病和其他人类脱髓鞘疾病，如多发性硬化症，可以解释为病毒和中枢神经系统（eNS）成分之间产生交叉反应的免疫反应。这些免疫应答将导致在患有这些疾病的个体中观察到的组织病理学和临床变化（FUJINAMI和OLDSTONE，1986，1987），并且是病毒感染，特别是麻疹病毒感染后的典型脑病。然而，很少从eNS中回收病毒，并且其存在与疾病的发生无关（米勒et al. 1956; AARLI 1974; ApPLEBAUM et al. 1949）;因此不太可能直接由病毒引起的组织破坏。
It has long been speculated that viruses share cross-reacting determinants with their host self-components. Not until recently could this be directly demonstrated by using monoclonal antibodies (Mabs) and by making direct protein sequence comparisons. This concept of shared common determinants has been the basis for understanding the mechanisms of virus-induced autoimmunity. The encephalomyelopathies following virus infection and other human demyelinating diseases, such as multiple sclerosis, may be explained by the generation of cross-reacting immune responses between viruses and central nervous system (eNS) components. These immune responses would be responsible for the histopathologic and clinical changes observed in individuals with these diseases (FUJINAMI and OLDSTONE, 1986, 1987) and typical of encephalopathies that follow viral infections, particularly infection with measles virus. However, virus is rearely recovered from the eNS, and its presence does not correlate with occurrence of disease (MILLER et al. 1956; AARLI 1974; ApPLEBAUM et al. 1949); thus direct, virally caused tissue destruction is unlikely.