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首页> 外文期刊>Infection and immunity >Immunization of Aotus nancymai with recombinant C terminus of Plasmodium falciparum merozoite surface protein 1 in liposomes and alum adjuvant does not induce protection against a challenge infection.
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Immunization of Aotus nancymai with recombinant C terminus of Plasmodium falciparum merozoite surface protein 1 in liposomes and alum adjuvant does not induce protection against a challenge infection.

机译：Aotus Nancymai与脂质体和alum佐剂中疟原虫的重组C末端的疟原物C末端不会导致防止攻击感染的保护。

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摘要

Merozoite surface protein 1 (MSP-1) of Plasmodium falciparum is an antimalarial vaccine candidate. The highly conserved 19-kDa C-terminal processing fragment of MSP-1 (MSP-1(19)) is of particular interest since it contains epitopes recognized by monoclonal antibodies which inhibit the invasion of erythrocytes in vitro. The presence of naturally acquired anti-MSP-1(19) antibodies in individuals exposed to malaria has been correlated with reduced morbidity, and immunization with an equivalent recombinant P. yoelii antigen induces substantial protection against this parasite in mice. We have expressed P. falciparum MSP-1(19) in Escherichia coli as a correctly folded protein and immunized Aotus nancymai monkeys by using the protein incorporated into liposomes and adsorbed to alum. After vaccination, the sera from these animals contained anti-MSP-1(19) antibodies, some of which competed for binding to MSP-1(19) with monoclonal antibodies that inhibit parasite invasion of erythrocytes in vitro. However, after challenge with either a homologous or a heterologous strain of parasite, all animals became parasitemic and required treatment. The immunization did not induce protection in this animal model.
机译：Merozoite Falciparum疟原虫的表面蛋白1（MSP-1）是抗疟疾疫苗候选者。 MSP-1（MSP-1（19））的高度保守的19-KDA C末端处理片段特别感兴趣，因为它含有通过单克隆抗体识别的表位，其抑制体外侵入红细胞的侵袭。在暴露于疟疾暴露于疟疾的个体中的天然所获得的抗MSP-1（19）抗体已经与降低的发病率相关，并且用当量重组P. yoelii抗原免疫诱导小鼠寄生虫的大量保护。我们通过使用掺入脂质体的蛋白质并吸附到明矾的蛋白质，在大肠杆菌中表达了对大肠杆菌的蛋白质和免疫蛋白质猴子的P.Malciparum MSP-1（19）。接种疫苗后，来自这些动物的血清含有抗MSP-1（19）抗体，其中一些抗体与单克隆抗体竞争与MSP-1（19）的结合，所述单克隆抗体抑制寄生虫侵袭性在体外寄生虫侵袭。然而，在用同源或异源寄生虫的寄生虫的攻击之后，所有动物都变成了寄生和所需的治疗。免疫没有在这种动物模型中诱导保护。

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