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首页> 外文期刊>Infection and immunity >Splenic requirement for antigenic variation and expression of the variant antigen on the erythrocyte membrane in cloned Plasmodium knowlesi malaria.
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Splenic requirement for antigenic variation and expression of the variant antigen on the erythrocyte membrane in cloned Plasmodium knowlesi malaria.

机译：克隆的知识型疟原虫疟疾的抗原变异和变异抗原在红细胞膜上表达的脾功能需求。

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Variant antigens appear on the surface of Plasmodium knowlesi-infected erythrocytes as the asexual parasite matures and are detected by antibody-mediated schizont-infected cell agglutination (SICA). We now show that cloned parasites can undergo antigenic variation in nonsplenectomized monkeys. In addition, we previously described a new P. knowlesi phenotype in which uncloned parasites passaged in splenectomized monkeys were no longer agglutinable by immune sera. We have designated this new phenotype SICA[-] and the one expressing the variant antigen SICA[+]. Cloned parasites can also switch from SICA[+] to SICA[-] in splenectomized monkeys. The switch from SICA[+] to SICA[-] is a gradual process that requires sequential subpassage in several monkeys. After passage in one monkey, the agglutination titer decreased 4- to 16-fold. Decreased agglutination was associated with decreased antibody binding on all infected erythrocytes as measured by fluorescein-conjugated anti-rhesus monkey immunoglobulin. The asexual malaria parasite can therefore alter its expression of variant antigen in response to the host environment (antivariant antibody or splenectomy). When cloned SICA[-] parasites were inoculated into intact monkeys, two courses of parasitemia were observed: fulminant parasitemia (greater than 20%) and parasitemia that was controlled. Fulminant infections were associated with conversion of the parasite from SICA[-] to SICA[+], i.e., from nonexpression to expression of the variant antigen on the erythrocyte surface. Parasitized erythrocytes remained SICA[-] in those infections that were controlled. It appears, therefore, that the expression of the variant antigen on the erythrocyte surface may influence parasite virulence.
机译：随着无性寄生虫的成熟，变异抗原出现在诺氏疟原虫感染的红细胞表面，并通过抗体介导的裂殖体感染细胞凝集（SICA）检测到。现在我们显示克隆的寄生虫可以在未脾切除的猴子中发生抗原变异。此外，我们先前描述了一种新的诺氏疟原虫表型，其中在脾切除的猴子中传代的未克隆寄生虫不再能被免疫血清凝集。我们指定了这种新的表型SICA [-]和表达变异抗原SICA [+]的表型。在脾切除的猴子中，克隆的寄生虫也可以从SICA [+]转换为SICA [-]。从SICA [+]到SICA [-]的转换是一个渐进过程，需要在几只猴子中进行顺序子通道传递。在一只猴子中传代后，凝集滴度降低了4至16倍。通过荧光素缀合的抗恒河猴免疫球蛋白测定，凝集减少与抗体在所有感染红细胞上的结合减少有关。因此，无性疟原虫可以响应宿主环境（抗变异抗体或脾切除术）改变其变异抗原的表达。将克隆的SICA [-]寄生虫接种到完整的猴子中后，观察到两个寄生虫病过程：暴发性寄生虫病（大于20％）和可控制的寄生虫病。暴发性感染与寄生虫从SICA [-]到SICA [+]的转化有关，即从未表达到变体抗原在红细胞表面的表达。在被控制的那些感染中，被寄生的红细胞仍然是SICA [-]。因此，看来变体抗原在红细胞表面上的表达可能影响寄生虫毒力。

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