Rodriguez M, Lafuse W P, Leibowitz J, David C S
Neurology. 1986 Jul;36(7):964-70. doi: 10.1212/wnl.36.7.964.
In vivo administration of monoclonal antibody reactive with major histocompatibility complex-encoded Ia molecules (I-As) partially suppressed inflammation and demyelination in the spinal cord of SJL/J (H-2s) mice persistently infected with Theiler's murine encephalomyelitis virus. Demyelination was decreased if antibody was given at the time of virus inoculation or after inflammation had been established in the spinal cord. The decrease in demyelination was independent of isolation of infectious virus from the CNS or of serum titers of immunoglobulin to purified viral antigen. Thus, Theiler's virus-induced demyelination is mediated, in part, by immune cells that carry Ia class II molecules.
给与针对主要组织相容性复合体编码的Ia分子(I-As)的单克隆抗体进行体内给药,部分抑制了持续感染泰勒氏鼠脑脊髓炎病毒的SJL/J(H-2s)小鼠脊髓中的炎症和脱髓鞘。如果在病毒接种时或脊髓炎症形成后给予抗体,脱髓鞘会减少。脱髓鞘的减少与从CNS中分离出感染性病毒或针对纯化病毒抗原的免疫球蛋白血清滴度无关。因此,泰勒氏病毒诱导的脱髓鞘部分是由携带II类Ia分子的免疫细胞介导的。