Tissue culture demyelination by normal human serum.
Tissue culture demyelination by normal human serum.
复制标题
通过正常人血清进行组织培养脱髓鞘。
DOI：
10.1002/ana.410150610
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发表时间：
1984
影响因子：
11.2
通讯作者：
Schreiber,AD
中科院分区：
文献类型：
--
作者：
Silberberg,DH;Manning,MC;Schreiber,AD
将所有20名正常人的血清应用于髓鞘良好的小鼠小脑培养，均可引起一定程度的脱髓鞘。需要完整的补体序列，直到C5。脱髓鞘活性在56℃下30分钟是热不稳定的，但在50℃下30分钟不会破坏(这会抑制备解素B和交替补体途径的激活，但不会抑制经典的补体途径)。无丙种球蛋白血症、C4缺乏症或C6缺乏症患者的血清均可引起脱髓鞘。我们的结果表明，组织培养脱髓鞘是由替代补体途径的非免疫球蛋白激活引起的，而且并不局限于神经系统疾病患者的血清。
Serum from all of 20 normal individuals induced some degree of demyelination when applied to well‐myelinated mouse cerebellum cultures. An intact complement sequence through C5 is required. Demyelinating activity was heat labile at 56°C for 30 minutes but was not destroyed at 50°C for 30 minutes (which inhibits properdin factor B and alternate complement pathway activation, but not the classic complement pathway). Sera from patients with agammaglobulinemia, C4 deficiency, or C6 deficiency all induced demyelination. Our results suggest that tissue culture demyelination results from nonimmunoglobulin activation of the alternate complement pathway and is not limited to sera from patients with neurological disease.