Murphy J R, Logie P S
Am J Trop Med Hyg. 1984 May;33(3):347-56. doi: 10.4269/ajtmh.1984.33.347.
Humoral immunity to Plasmodium berghei infection of F1 hybrid B6D2 (C57B1/6 X DBA/2) mice was investigated using an immune serum prepared from mice which survived a lethal challenge of erythrocytic stage P. berghei because of previous vaccination with formalin-killed P. berghei. Immune serum, but not normal serum, if injected intraperitoneally or intravenously soon after infection, during rapidly increasing parasitemia, transiently inhibited the progress of infection in a pattern which was directly related to the dose and timing of serum injection. However, the level of restriction of parasitemia caused by the intravenous injection of 1 ml of immune serum could not be improved upon by subsequent additional 1-ml injections of the same serum, and parasitemia in all mice, whether delayed by immune serum or not, ultimately progressed to death. The protective capacity of the immune serum was markedly specific for plasmodial species but absorption with formalin-killed homologous parasites failed to remove the protective component. No variants of P. berghei insensitive to inhibition by immune serum were detected. The results support the view that humoral immunity to P. berghei may be mediated by more than one soluble factor and effected through at least two different pathways.
利用从因先前接种福尔马林灭活的伯氏疟原虫而在红细胞期伯氏疟原虫致死性攻击中存活下来的小鼠制备的免疫血清，研究了F1杂交B6D2（C57B1/6×DBA/2）小鼠对伯氏疟原虫感染的体液免疫。在感染后不久、疟原虫血症迅速增加期间，腹腔内或静脉内注射免疫血清而非正常血清，会以一种与血清注射剂量和时间直接相关的模式短暂抑制感染进程。然而，静脉注射1毫升免疫血清所引起的疟原虫血症限制水平，不会因随后再注射1毫升相同血清而得到改善，并且所有小鼠的疟原虫血症，无论是否被免疫血清延迟，最终都会发展至死亡。免疫血清的保护能力对疟原虫种类具有明显的特异性，但用福尔马林灭活的同源寄生虫进行吸收并不能去除保护成分。未检测到对免疫血清抑制不敏感的伯氏疟原虫变体。这些结果支持这样一种观点，即对伯氏疟原虫的体液免疫可能由不止一种可溶性因子介导，并通过至少两种不同途径实现。
