Schetters T P, Van Run van Breda J H, Hermsen C, Curfs J, Eling W M
Department of Cytology and Histology, University of Nijmegen, The Netherlands.
Parasite Immunol. 1989 Jul;11(4):413-23. doi: 10.1111/j.1365-3024.1989.tb00678.x.
The serum from mice developing resistance against Plasmodium berghei infection using chemotherapeutic treatment has been analysed in vivo and in vitro. During the immunization period pathological as well as protective activities which could be transferred by serum were generated. The pathological activity, which was defined as destruction of erythrocytes in normal recipient mice, was generated early in the immunization procedure, peaked at day 21, and decreased to undetectable levels by day 35. After reinfection of the donor mice the pathological activity reappeared in the serum, and was maintained for at least 56 days. Analysis of the transferred serum samples showed the presence of anti-erythrocyte antibodies (ELISA), but no correlation with the in-vivo anti-erythrocyte effect could be found. The anti-erythrocyte effect of the serum samples indirectly increased the parasitaemia in the recipient mice through the induction of reticulocytosis. The protective effect of the serum samples could only be detected in samples taken from animals beyond day 61 of the immunization procedure. This net protective effect was reflected in a decreased parasitaemia at 7 days after challenge of the recipient mice with P. berghei infected erythrocytes. The protective activity of the serum was correlated with high titres of anti-erythrocyte antibodies. Anti-erythrocyte antibody titres were strongly correlated with titres against heterologous red blood cells as well as total immunoglobulin content of the serum samples, indicative of polyclonal activation of lymphocytes. Except for IgG1, all (sub-)classes were elevated during the immunization procedure, of which IgG3 was abundant. After immunity was obtained these immunoglobulin levels remained high, and the relative amount of IgG1 in the serum was restored.
已对使用化疗治疗产生抗伯氏疟原虫感染抗性的小鼠血清进行了体内和体外分析。在免疫期间，产生了可通过血清转移的病理以及保护活性。病理活性定义为正常受体小鼠中红细胞的破坏，在免疫过程早期产生，在第21天达到峰值，并在第35天降至无法检测的水平。供体小鼠再次感染后，病理活性在血清中重新出现，并维持至少56天。对转移的血清样本分析显示存在抗红细胞抗体（ELISA），但未发现与体内抗红细胞效应有相关性。血清样本的抗红细胞效应通过诱导网织红细胞增多间接增加了受体小鼠的寄生虫血症。血清样本的保护作用仅在免疫程序第61天之后采集的样本中才能检测到。这种净保护作用表现为受体小鼠用感染伯氏疟原虫的红细胞攻击7天后寄生虫血症降低。血清的保护活性与高滴度的抗红细胞抗体相关。抗红细胞抗体滴度与针对异源红细胞的滴度以及血清样本的总免疫球蛋白含量密切相关，表明淋巴细胞的多克隆激活。除IgG1外，所有（亚）类在免疫过程中均升高，其中IgG3含量丰富。获得免疫力后，这些免疫球蛋白水平仍然很高，血清中IgG1的相对量得以恢复。
