Jarra W, Hills L A, March J C, Brown K N
Parasite Immunol. 1986 May;8(3):239-54. doi: 10.1111/j.1365-3024.1986.tb01036.x.
Serum was obtained from CBA/Ca mice infected, reinfected or superinfected with parasites taken one or two syringe passages from cryopreserved reference stabilates derived from cloned lines of the AS or CB isolates of P.c. chabaudi. Serum was also collected from mice superinfected with parasites derived from a cloned line of P. berghei KSP-11. When injected into normal syngeneic recipients subsequently challenged with homologous or heterologous parasites, these sera mediated some or all of the following modifications to the breakthrough parasitaemias which invariably occurred (i) an extension of the pre-patent period (ii) an extension of the time taken for the parasitaemia to reach 2% (iii) a reduction of peak parasitaemia (iv) protraction of the initial peak of parasitaemia. These modifications were particularly evident with serum from superinfected mice and to a lesser extent with serum from animals reinfected once after recovery from a primary infection. Serum taken during the course of such a primary infection produced extended pre-2% periods, other effects being only marginal. Serum mediated modifications produced by reinfection and superinfection serum appeared largely species-specific with a limited degree of cross-reactivity. Intraspecific specificity was also apparent with serum from P.c. chabaudi AS or CB reinfected or superinfected mice, although marginal cross-immunity was again observed. When analysed by the fluorescent antibody technique on smears of methanol fixed parasitized erythrocytes, reinfection and superinfection sera were almost totally cross-reactive both within and across species. Preliminary evidence that parasites breaking through the effects of these sera may constitute a phenotypic antigenic variant is presented and possible mechanisms for the parasitaemia modifying effects of the various sera discussed.
从感染、再次感染或超感染寄生虫的CBA/Ca小鼠中获取血清,这些寄生虫取自从约氏疟原虫AS或CB分离株的克隆系的冷冻保存参考稳定株经一或两次注射器传代培养的样本。还从感染了伯氏疟原虫KSP-11克隆系来源的寄生虫的小鼠中收集血清。当将这些血清注射到随后用同源或异源寄生虫攻击的正常同基因受体中时,这些血清对总是会出现的突破期寄生虫血症产生了以下部分或全部改变:(i) 潜伏期延长;(ii) 寄生虫血症达到2%所需时间延长;(iii) 峰值寄生虫血症降低;(iv) 寄生虫血症初始峰值延长。这些改变在超感染小鼠的血清中尤为明显,而在初次感染恢复后再次感染的动物血清中程度较轻。在这种初次感染过程中采集的血清产生了延长的2%之前的时期,其他影响仅为轻微。再次感染和超感染血清介导的改变在很大程度上具有种属特异性,交叉反应程度有限。约氏疟原虫AS或CB再次感染或超感染小鼠的血清中也表现出种内特异性,尽管再次观察到了轻微的交叉免疫。当通过荧光抗体技术在甲醇固定的寄生红细胞涂片上进行分析时,再次感染和超感染血清在种内和种间几乎完全交叉反应。提出了初步证据表明突破这些血清作用的寄生虫可能构成表型抗原变异体,并讨论了各种血清对寄生虫血症产生修饰作用的可能机制。