Plasmodium falciparum: Differential parasite growth inhibition mediated by antibodies to the antigens Pf332 and Pf155/RESA
Plasmodium falciparum: Differential parasite growth inhibition mediated by antibodies to the antigens Pf332 and Pf155/RESA
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DOI：
10.1006/expr.1996.0020
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发表时间：
1996-03-01
影响因子：
2.1
通讯作者：
Berzins, K
中科院分区：
文献类型：
--
作者：
Ahlborg, N;Iqbal, J;Berzins, K
恶性疟原虫反应性抗体可以通过干扰寄生虫发育的不同阶段来抑制体外寄生虫血液阶段的生长。与Pf 155/环感染表面抗原（Pf 155/RESA）或抗原Pf 332中的重复序列反应的抗体抑制寄生虫生长，如通过减少新感染的红细胞所确定的。Pf 155/RESA抗体与裂殖子侵袭抑制有关。由于认为晚期抗原Pf 332的抗体不太可能作用于裂殖子入侵，我们研究了这种生长抑制发生在什么发育阶段。寄生虫培养的抗体的存在下，以重复序列的Pf 332或Pf 155/ RESA和检查方面的不同阶段的分布和它们的形态。正如预期的那样，两种抗原的抗体减少了再感染后的环阶段的数量。它们不影响红细胞内发育的环形阶段或滋养体。然而，Pf 332的抗体诱导高水平的显示异常形态的树突，而Pf 155/RESA的抗体诱导相当低水平的退化树突。因此，Pf 332-反应性抗体似乎通过阻断成熟疟原虫的破裂或通过干扰红细胞内晚期寄生虫来干扰疟原虫的发育。(C)出版社：Academic Press，Inc.
Plasmodium falciparum-reactive antibodies can inhibit growth of parasite blood stages in vitro by interfering at different stages of parasite development. Antibodies reactive with repeat sequences in Pf155/ring-infected surface antigen (Pf155/RESA) or in antigen Pf332 inhibit parasite growth as determined by a reduction of newly infected erythrocytes. Antibodies to Pf155/RESA have been implicated in merozoite invasion inhibition. Since it was considered unlikely that antibodies to the late stage antigen Pf332 act on merozoite invasion, we investigated at what developmental stage this growth inhibition takes place. Parasites were cultured in the presence of antibodies to repeat sequences of either Pf332 or Pf155/ RESA and were examined with regard to the distribution of different stages and their morphology. As expected, antibodies to both antigens decreased the number of ring stages after reinfection. They did not affect the intraerythrocytic development of ring stages or trophozoites. However, antibodies to Pf332 induced high levels of schizonts displaying an abnormal morphology while antibodies to Pf155/RESA induced considerably lower levels of degenerated schizonts. Thus, Pf332-reactive antibodies seem to interfere with the schizont development by blocking the rupture of mature schizonts or, alternatively, by interfering intraerythrocytically with late stage parasites. (C) 1996 Academic Press, Inc.