Antibodies Reactive with the N-Terminal Domain ofPlasmodium falciparum Serine Repeat Antigen Inhibit Cell Proliferation by Agglutinating Merozoites and Schizonts
Antibodies Reactive with the N-Terminal Domain ofPlasmodium falciparum Serine Repeat Antigen Inhibit Cell Proliferation by Agglutinating Merozoites and Schizonts
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与恶性疟原虫丝氨酸重复抗原 N 端结构域反应的抗体通过凝集裂殖子和裂殖体抑制细胞增殖
作者：
X. Pang;T. Mitamura;T. Horii
恶性疟原虫丝氨酸重复序列抗原（serine repeat antigen，SERA）是恶性疟原虫疫苗的候选抗原。用大肠杆菌SERA N端结构域（SE47 ′）重组蛋白免疫小鼠，可诱导出抗血清，在体外对寄生虫的生长有抑制作用。亲和纯化的重组蛋白特异性的小鼠抗体抑制寄生虫的生长之间的寄生虫和环形阶段，但不之间的环形和寄生虫阶段。当Percoll纯化的裂殖子与亲和纯化的SE47 ′特异性抗体一起培养时，裂殖子和裂殖子凝集。用未固定的寄生虫细胞进行的间接免疫荧光试验表明，SE47 ′特异性免疫球蛋白G（IgG）与破裂的寄生虫和裂殖子上的SERA分子结合，但IgG不与寄生虫感染的红细胞（RBC）反应。用SE47 ′特异性IgG和抗人红细胞膜IgG双荧光染色法检测，培养后红细胞膜从SE47 ′特异性IgG结合的载体上消失。这些观察结果表明，SE47 ′特异性抗体通过交联SERA分子抑制寄生虫生长，SERA分子与裂殖子相关，在破裂的带有部分破裂的RBC和寄生虫空泡膜的寄生虫中，阻断裂殖子释放。
ABSTRACT The serine repeat antigen (SERA) is a vaccine candidate antigen ofPlasmodium falciparum. Immunization of mice withEscherichia coli-produced recombinant protein of the SERA N-terminal domain (SE47′) induced an antiserum that was inhibitory to parasite growth in vitro. Affinity-purified mouse antibodies specific to the recombinant protein inhibited parasite growth between the schizont and ring stages but not between the ring and schizont stages. When Percoll-purified schizonts were cultured with the affinity-purified SE47′-specific antibodies, schizonts and merozoites were agglutinated. Indirect-immunofluorescence assays with unfixed parasite cells showed that SE47′-specific immunoglobulin G (IgG) bound to SERA molecules on rupturing schizonts and merozoites but the IgG did not react with the schizont-infected erythrocytes (RBC). Furthermore, double-fluorescence staining against SE47′-specific IgG and anti-human RBC membrane IgG showed that the RBC membrane disappeared from SE47′-specific-IgG-bound schizonts after cultivation. These observations suggest that the SE47′-specific antibodies inhibit parasite growth by cross-linking SERA molecules that are associated with merozoites in rupturing schizonts with partly broken RBC and parasitophorous vacuole membranes, blocking merozoite release.
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