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脱髓鞘疾病的组织培养研究:批判性综述。

Tissue culture studies of demyelinating disease: a critical review.

作者信息

Seil F J

出版信息

Ann Neurol. 1977 Oct;2(4):345-55. doi: 10.1002/ana.410020417.

Abstract

Tissue culture studies of human and experimental demyelinating diseases have demonstrated that sera from patients with multiple sclerosis reversibly demyelinate central nervous system cultures. Similar changes are evoked by sera from animals with experimental allergic encephalomyelitis induced by inoculation with whole central nervous system tissue but not by encephalitogenic myelin basic protein. Sera and buffy coat or lymph node cells from humans with idiopathic polyneuritis and animals with experimental allergic neuritis demyelinate cultures of peripheral nervous system tissue. While these studies have contributed to speculations about pathogenetic mechanisms of demyelinating diseases, including the role of both circulating antibodies and delayed hypersensitivity factors, a number of important questions remain unanswered. Among these are the identity of the antigens that evoke antimyelin antibodies and the precise relationship of serum or cellular antimyelin factors to the pathogenesis or clinical course of the demyelinating diseases. Further studies with this technique may provide more complete information about the role of immunological events in induction of disease.

摘要

对人类和实验性脱髓鞘疾病的组织培养研究表明,多发性硬化症患者的血清可使中枢神经系统培养物发生可逆性脱髓鞘。接种全中枢神经系统组织诱导的实验性变应性脑脊髓炎动物的血清也会引起类似变化,但致脑炎的髓鞘碱性蛋白则不会。特发性多神经炎患者以及实验性变应性神经炎动物的血清、血沉棕黄层或淋巴结细胞会使周围神经系统组织培养物发生脱髓鞘。虽然这些研究有助于推测脱髓鞘疾病的发病机制,包括循环抗体和迟发型超敏反应因子的作用,但仍有许多重要问题未得到解答。其中包括引发抗髓鞘抗体的抗原的身份,以及血清或细胞抗髓鞘因子与脱髓鞘疾病的发病机制或临床病程的确切关系。使用该技术进行的进一步研究可能会提供关于免疫事件在疾病诱导中的作用的更完整信息。

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