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Immune pressure selects for Plasmodium falciparum parasites presenting distinct red blood cell surface antigens and inducing strain-specific protection in Saimiri sciureus monkeys

机译:免疫压力选择恶性疟原虫的寄生虫,这些寄生虫呈现出独特的红细胞表面抗原并诱导赛密尔猴(Saimiri sciureus)猴子产生菌株特异性保护

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摘要

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.
机译:特异性抗体的被动转移到天真的脾脏切除的Saimiri sciureus猴身上,该猴感染了恶性疟原虫的Palo Alto FUP / SP菌株,导致出现了对转移的抗体有抗性的寄生虫。分子分型表明原始和抗性寄生虫是等基因的。原始寄生虫致病的赛米瑞猴完全容易受到抗药性动物的攻击,反之亦然。这种交叉保护的缺乏表明,菌株特异性决定簇将是这些猴子中发展的保护性免疫的主要靶标。表型分析表明,在两个品系中,受感染的红细胞表面均不同。原始的寄生虫形成玫瑰花结,自动凝集,在被感染的红细胞表面呈现特征性的结节,并且在存在人类免疫血清池的情况下不凝集。相反,在存在人类免疫血清的情况下,抗药性寄生虫不会形成玫瑰花结,不会自发自凝集,不会出现异常扁平的结节,并且会形成较大的聚集体。通过表面免疫荧光和使用同源Saimiri血清的凝集证实了在抗性寄生虫表面上菌株特异性决定簇的存在。原始的和抗药性的寄生虫都没有细胞粘附于黑色素瘤黑素瘤细胞系,这表明细胞粘附和凝集作用可以被解离。这些结果表明,由于暴露于红细胞表面的抗原而不同的寄生虫诱导了菌株特异性免疫。此外,它们显示玫瑰花结和非结实寄生虫的抗原特性不同,并且不会交叉保护。

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