Antigenic variation of cloned Plasmodium fragile in its natural host Macaca sinica. Sequential appearance of successive variant antigenic types.

Antigenic variation of cloned Plasmodium fragile in its natural host Macaca sinica. Sequential appearance of successive variant antigenic types.
复制标题

DOI:
10.1084/jem.165.5.1269
复制
发表时间:
1987-05-01
期刊:
The Journal of experimental medicine
影响因子:
--
通讯作者:
David PH
David PH
中科院分区:
其他
文献类型:
--
作者:
Handunnetti SM;Mendis KN;David PH

文献摘要

被引文献

相似文献

脆弱疟原虫在其自然宿主猕猴体内的感染过程包括寄生虫血症的第一个高峰,随后是几个不同的、连续的低级寄生虫血症高峰。在S+宿主中,脆性变形杆菌红细胞内无性发育晚期诱导感染红细胞表面抗原的表达,这可以使用表面免疫荧光技术检测。使用悬浮液中的未固定红细胞的免疫荧光显示,抗原被感染了更成熟阶段的寄生虫的红细胞表面上的免疫血清识别。这些抗原发生变异,寄生虫血症的每个连续峰的特征在于不同的变异抗原型(VAT)。连续的增值税的出现发生在一个连续的方式,遵循相同的顺序在不同的动物。这构成了疟原虫中抗原连续表达的第一个例子;它表明,在脆弱疟原虫中,抗原变异不是抗体选择的随机突变的结果。在S-宿主中不能检测到感染红细胞表面的寄生虫诱导抗原。然而,当非表达寄生虫从S-主机被转移到一个幼稚的S+动物的血液通道,他们开始在两个红细胞周期内感染的红细胞表面上表达抗原。我们已经证明,在S-动物感染过程中,S-寄生虫在传代到S+动物中时切换到特定VAT的能力发生变化,这表明,尽管表面抗原不表达,但导致抗原变异的过程甚至发生在S-宿主中。针对这些表面抗原的抗体抑制红细胞内寄生虫的生长。抗体的生长抑制作用也是变体特异性的,表明这些变体表面抗原对寄生虫存活具有重要的功能。
The course of infection of Plasmodium fragile in its natural host, the toque monkey Macaca sinica, consists of a primary peak of parasitemia followed by several distinct, successive peaks of lower parasitemia. In the S+ host, the late intraerythrocytic asexual developmental stages of P. fragile induce the expression of antigens on the surface of infected erythrocytes, which could be detected using the technique of surface immunofluorescence. Immunofluorescence using unfixed erythrocytes in suspension has shown that antigens are recognized by immune serum on the surface of the erythrocytes infected with more mature stages of the parasite. These antigens undergo variation, each successive peak of parasitemia being characterized by a different variant antigenic type (VAT). The appearance of the successive VATs occurs in a sequential manner, following the same order in different sets of animals. This constitutes the first example of a sequential expression of antigens in a malaria parasite; it indicates that, in P. fragile, antigenic variation is not the result of random mutations selected by antibody. Parasite-induced antigens on the surface of infected erythrocytes could not be detected in the S- host. However, when nonexpressing parasites from the S- host were transferred by blood passage into a naive S+ animal, they began to express antigens on the surface of infected erythrocytes within two erythrocytic cycles. We have demonstrated that the ability of S- parasites to switch to a particular VAT when passaged into a S+ animal changes during the course of an infection in the S- animal, indicating that, although surface antigens are not expressed, the processes leading to antigenic variation occurs even in the S- host. Antibodies directed against these surface antigens inhibit the growth of intra-erythrocytic parasites. The growth inhibition effects of antibodies are also variant specific, indicating that these variant surface antigens are functionally important for parasite survival.