Silberberg D H, Manning M C, Schreiber A D
Ann Neurol. 1984 Jun;15(6):575-80. doi: 10.1002/ana.410150610.
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 degrees C for 30 minutes but was not destroyed at 50 degrees 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.
来自20名正常个体的血清,当应用于髓鞘形成良好的小鼠小脑培养物时,均会诱导一定程度的脱髓鞘。需要完整的补体序列直至C5。脱髓鞘活性在56℃加热30分钟时不稳定,但在50℃加热30分钟时不会被破坏(50℃加热30分钟可抑制备解素因子B和替代补体途径的激活,但不影响经典补体途径)。无丙种球蛋白血症、C4缺乏或C6缺乏患者的血清均能诱导脱髓鞘。我们的结果表明,组织培养中的脱髓鞘是由替代补体途径的非免疫球蛋白激活引起的,并不局限于神经疾病患者的血清。