Lassmann H, Stemberger H, Kitz K, Wisniewski H M
J Neurol Sci. 1983 Apr;59(1):123-37. doi: 10.1016/0022-510x(83)90086-2.
Sera from guinea pigs and rats with chronic experimental allergic encephalomyelitis were injected into the cerebrospinal fluid (CSF) of normal recipient rats. Guinea pig sera induced demyelination in the central and (or) peripheral nervous system, whereas injection of rat sera resulted in demyelination in the peripheral nervous system only. Control sera did not induce demyelination. Demyelinating activity in guinea pig sera was confined to the IgG-fraction; in rat sera the IgG- as well as the IgM-fraction were able to induce demyelination. The demyelinating activity was abolished when the sera were absorbed with with sensitising antigen (guinea pig spinal cord tissue) or when immunoglobulins were removed from the sera. When chronic EAE sera from rats were injected into the CSF of rats, complement was not required for the induction of demyeLination. The presence of complement, however, augmented the demyelinating activity. Decomplemented chronic EAE sera from guinea pigs failed to induce demyelination after injection into the CSF of rats. Injection of control and non-demyelinating or demyelinating EAE sera into the subarachnoid space of normal recipient rats induced a weak inflammatory response with increased numbers of large mononuclear cells in the meninges. It is discussed that in vivo a complex interaction of antibodies, complement and effector cells is responsible for induction of demyelination.
将患有慢性实验性变应性脑脊髓炎的豚鼠和大鼠的血清注入正常受体大鼠的脑脊液（CSF）中。豚鼠血清可诱导中枢和（或）外周神经系统脱髓鞘，而注射大鼠血清仅导致外周神经系统脱髓鞘。对照血清未诱导脱髓鞘。豚鼠血清中的脱髓鞘活性局限于IgG组分；在大鼠血清中，IgG以及IgM组分均能够诱导脱髓鞘。当血清用致敏抗原（豚鼠脊髓组织）吸收或从血清中去除免疫球蛋白时，脱髓鞘活性消失。当将大鼠的慢性实验性变应性脑脊髓炎血清注入大鼠的脑脊液中时，诱导脱髓鞘不需要补体。然而，补体的存在增强了脱髓鞘活性。豚鼠的去补体慢性实验性变应性脑脊髓炎血清注入大鼠脑脊液后未能诱导脱髓鞘。将对照血清以及非脱髓鞘或脱髓鞘的实验性变应性脑脊髓炎血清注入正常受体大鼠的蛛网膜下腔，可诱导轻微的炎症反应，脑膜中大型单核细胞数量增加。有观点认为，在体内抗体、补体和效应细胞之间的复杂相互作用是诱导脱髓鞘的原因。
