Feasby T E, Hahn A F, Gilbert J J
Neurology. 1982 Oct;32(10):1159-67. doi: 10.1212/wnl.32.10.1151-a.
Serum and lymphocytes from patients with acute Guillain-Barré polyneuropathy were injected into rat sciatic nerves. Serum from 13 of 17 patients produced perivenular demyelination, associated with lymphocytic infiltration. The pattern of demyelination differed from that caused by experimental allergic neuritis serum. The level of serum demyelinating activity as greatest early in the disease and then decreased. The demyelinating factor was heat-labile but not complement-dependent. Circulating lymphocytes did not cause demyelination in eight patients.
将急性吉兰-巴雷综合征患者的血清和淋巴细胞注入大鼠坐骨神经。17例患者中有13例的血清导致了血管周围脱髓鞘，并伴有淋巴细胞浸润。脱髓鞘模式与实验性过敏性神经炎血清所致的不同。血清脱髓鞘活性水平在疾病早期最高，然后下降。脱髓鞘因子对热不稳定，但不依赖补体。8例患者的循环淋巴细胞未引起脱髓鞘。
