Fandeur T, Le Scanf C, Bonnemains B, Slomianny C, Mercereau-Puijalon O
Laboratoire de Parasitologie Moléculaire, Institut Pasteur de Guyane, Cayenne, French Guiana.
J Exp Med. 1995 Jan 1;181(1):283-95. doi: 10.1084/jem.181.1.283.
The passive transfer of specific antibodies to a naive splenectomized Saimiri sciureus monkey infected with the Palo Alto FUP/SP strain of Plasmodium falciparum resulted in the emergence of parasites resistant to the transferred antibodies. Molecular typing indicated that the original and resistant parasites were isogenic. Saimiri monkeys primed with original parasites were fully susceptible to a challenge by the resistant ones, and vice versa. This absence of crossprotection indicates that strain-specific determinants would be the major targets of protective immunity developed in these monkeys. Phenotypic analysis showed that the surface of the infected red blood cells differed in both lines. Original parasites formed rosettes, autoagglutinated, presented characteristic knobs at the surface of the infected red blood cell, and did not agglutinate in the presence of a pool of human immune sera. In contrast, the resistant parasites did not form rosettes, did not spontaneously autoagglutinate, presented abnormal flattened knobs, and formed large aggregates in the presence of a pool of human immune sera. The presence of strain-specific determinants at the surface of the resistant parasites was confirmed by surface immunofluorescence and agglutination using homologous Saimiri serum. Neither the original nor the resistant parasites cytoadhered to an amelanotic melanoma cell line, suggesting that cytoadherence and agglutination can be dissociated. These results indicate that parasites that differ by the antigens exposed at the surface of the red blood cell induce strain-specific immunity. Furthermore they show that rosetting and nonrosetting parasites differ in their antigenic properties and do not crossprotect.
将特异性抗体被动转移至感染恶性疟原虫帕洛阿尔托FUP/SP株的无脾松鼠猴体内，导致出现了对转移抗体具有抗性的寄生虫。分子分型表明，原始寄生虫和抗性寄生虫是同基因的。用原始寄生虫致敏的松鼠猴对抗性寄生虫的攻击完全易感，反之亦然。这种缺乏交叉保护的情况表明，菌株特异性决定簇将是这些猴子产生的保护性免疫的主要靶点。表型分析表明，两条谱系中感染红细胞的表面存在差异。原始寄生虫形成玫瑰花结、自身凝集，在感染红细胞表面呈现特征性的凸起，并且在人免疫血清池中不凝集。相比之下，抗性寄生虫不形成玫瑰花结，不自发自身凝集，呈现异常扁平的凸起，并且在人免疫血清池中形成大的聚集体。使用同源松鼠猴血清通过表面免疫荧光和凝集证实了抗性寄生虫表面存在菌株特异性决定簇。原始寄生虫和抗性寄生虫均未与无黑色素黑色素瘤细胞系发生细胞黏附，这表明细胞黏附和凝集可以分离。这些结果表明，红细胞表面暴露的抗原不同的寄生虫诱导菌株特异性免疫。此外，它们表明形成玫瑰花结和不形成玫瑰花结的寄生虫在抗原特性上存在差异，并且没有交叉保护作用。
