Hirsch R L, Griffin D E, Johnson R T
Infect Immun. 1979 Feb;23(2):320-4. doi: 10.1128/iai.23.2.320-324.1979.
Transfer of anti-Sindbis virus serum, obtained from peripherally inoculated donors, protected mice from an otherwise fatal intracerebral infection with neuroadapted Sindbis virus (NSV). F(ab)'2 preparations of serum were not protective, indicating that the Fc piece of immunoglobulin G was important. Complement-depleted animals were protected with anti-NSV serum, ruling out as essential the complement-fixing function of the Fc piece. The presence of protective antibody correlated with the ability of serum to inhibit T-cell cytotoxicity. However, experiments using athymic nude mice showed that T cells played no role in killing the mice since the 50% lethal dose was the same as that in normal BALB/c mice, and that T cells were not required for protection since athymic nude mice were protected with antibody alone. Cyclophosphamide treatment of NSV-infected mice ablated the protective capacity of anti-NSV serum. Therefore, a non-T cell, cyclophosphamide-sensitive cell was required for antibody-mediated protection.
从外周接种供体获得的抗辛德毕斯病毒血清可保护小鼠免受经神经适应的辛德毕斯病毒(NSV)致死性脑内感染。血清的F(ab)'2制剂没有保护作用,表明免疫球蛋白G的Fc片段很重要。用抗NSV血清可保护补体缺失的动物,排除了Fc片段的补体固定功能是必需的。保护性抗体的存在与血清抑制T细胞细胞毒性的能力相关。然而,使用无胸腺裸鼠的实验表明,T细胞在杀死小鼠中不起作用,因为50%致死剂量与正常BALB/c小鼠相同,并且由于无胸腺裸鼠仅用抗体就能得到保护,所以保护并不需要T细胞。用环磷酰胺处理NSV感染的小鼠消除了抗NSV血清的保护能力。因此,抗体介导的保护需要一种非T细胞、对环磷酰胺敏感的细胞。