Perlmann H, Berzins K, Wahlgren M, Carlsson J, Björkman A, Patarroyo M E, Perlmann P
J Exp Med. 1984 Jun 1;159(6):1686-704. doi: 10.1084/jem.159.6.1686.
Monolayers of human erythrocytes (E) infected with Plasmodium falciparum were briefly fixed with 1% glutaraldehyde and air dried. They were then exposed to sera from patients with P. falciparum malaria or from donors immune to this parasite and tested in an indirect immunofluorescence assay (IFA). Parasites in infected E were made visible by counterstaining with ethidium bromide. Immunofluorescence (IF) was restricted to the surface of infected E. No antibody binding was detected unless the E were dried, suggesting that the relevant antigens were not available on the outer layers of the E surface. Staining over large parts of the E surface was seen already when the merozoite penetrated noninfected cells and was strong in E containing early stages of the parasite (rings, trophozoites). It was weak or absent from E containing schizonts. Antibodies in sera from different parts of Africa, Colombia, or Sweden reacted similarly with E infected with a Tanzanian P. falciparum strain kept in culture for many years and with parasitized E freshly drawn from African, Swedish, or Colombian patients. All sera from residents of a holoendemic area (Liberia) were IFA positive. In contrast, some sera from Colombian or Swedish patients with primary infection gave negative results. The results of the IFA and of an enzyme-linked immunosorbent assay in which fixed and dried E were the targets were well-correlated, suggesting that the same antibodies were detected by these assays. The antigens involved in the IFA were susceptible to pronase but not to trypsin or neuraminidase. E surface IF was inhibited by lysates of infected E, merozoite extracts, or soluble antigens present in P. falciparum culture supernatants but not by lysates of normal E or ghost extracts. The inhibitory antigens were heat stable (100 degrees C, 5 min). Sodium dodecyl sulfate-polyacrylamide gel electrophoresis followed by immunoblotting of either antigen-enriched preparations from culture supernatants or merozoite extracts showed that antibodies eluted from monolayers of infected E reacted consistently with a predominant polypeptide of Mr 155,000 and two to four minor polypeptides of lower molecular weights. Metabolic labeling of the parasites with 75Se-methionine indicated that these antigens were parasite derived. We conclude that the antigens involved in these reactions are released from bursting schizonts or merozoites and are deposited in the E membrane in the course of invasion.(ABSTRACT TRUNCATED AT 400 WORDS)
用1%戊二醛对感染恶性疟原虫的人红细胞单层进行短暂固定并风干。然后将其暴露于恶性疟疾病人的血清或对该寄生虫免疫的供血者血清中,并在间接免疫荧光试验(IFA)中进行检测。用溴化乙锭复染使感染红细胞中的寄生虫可见。免疫荧光(IF)局限于感染红细胞的表面。除非红细胞被风干,否则未检测到抗体结合,这表明相关抗原在红细胞表面外层不可用。当裂殖子侵入未感染细胞时,在红细胞表面的大部分区域可见染色,并且在含有寄生虫早期阶段(环状体、滋养体)的红细胞中染色很强。在含有裂殖体的红细胞中染色较弱或无染色。来自非洲不同地区、哥伦比亚或瑞典的血清中的抗体,与感染了在培养中保存多年的坦桑尼亚恶性疟原虫菌株的红细胞以及从非洲、瑞典或哥伦比亚患者新鲜采集的被寄生红细胞反应相似。来自高度流行区(利比里亚)居民的所有血清IFA检测均为阳性。相比之下,一些来自哥伦比亚或瑞典初感染患者的血清结果为阴性。以固定和风干的红细胞为靶点的IFA和酶联免疫吸附试验结果相关性良好,表明这些试验检测到的是相同的抗体。IFA中涉及的抗原对链霉蛋白酶敏感,但对胰蛋白酶或神经氨酸酶不敏感。红细胞表面IF受到感染红细胞裂解物、裂殖子提取物或恶性疟原虫培养上清液中存在的可溶性抗原的抑制,但不受正常红细胞裂解物或空泡提取物的抑制。抑制性抗原热稳定(100℃,5分钟)。对培养上清液或裂殖子提取物中的抗原富集制剂进行十二烷基硫酸钠 - 聚丙烯酰胺凝胶电泳,然后进行免疫印迹分析,结果显示从感染红细胞单层洗脱的抗体与一条主要的分子量为155,000的多肽以及两到四条较低分子量的次要多肽一致反应。用75Se - 甲硫氨酸对寄生虫进行代谢标记表明这些抗原来源于寄生虫。我们得出结论,这些反应中涉及的抗原是从破裂的裂殖体或裂殖子释放出来的,并在入侵过程中沉积在红细胞膜中。(摘要截短于400字)