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首页> 外文期刊>Infection and immunity >Kinetics of Humoral and Memory B Cell Response Induced by the Plasmodium falciparum 19-Kilodalton Merozoite Surface Protein 1 in Mice
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Kinetics of Humoral and Memory B Cell Response Induced by the Plasmodium falciparum 19-Kilodalton Merozoite Surface Protein 1 in Mice

机译：恶性疟原虫19-Kilodalton裂殖子表面蛋白1诱导小鼠的体液和记忆B细胞反应的动力学。

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The 19-kDa carboxyl-terminal fragment of the merozoite surface protein-1 (MSP-119) has been shown to regulate antibody (Ab)-mediated protective immunity to blood-stage malaria infection. But the serological memory to this antigen tends to be short-lived, and little is known of the mechanisms that regulate the formation of B cell memory to MSP-119 antigen. We studied the formation of B cell memory response after immunization with the recombinant 19-kDa Plasmodium falciparum merozoite surface protein 1 (PfMSP-119). Immunization with PfMSP-119 resulted in delayed increase in germinal center (GC) B cell numbers. This poor GC reaction correlated with short-lived PfMSP-119-specific antibodies in serum and the short life of PfMSP-119-specific plasma cells and memory B cells (MBCs) in spleen and bone marrow. PfMSP-119-specific MBCs were capable of producing antigen (Ag)-specific Ab-secreting cell (ASC) responses that were short-lived following challenge immunization of the immune mice with antigen or transgenic Plasmodium berghei parasite expressing PfMSP-119 in place of native P. berghei MSP-119 at 8 weeks after the last immunization or following adoptive transfer into naive hosts. However, no protection was achieved in PfMSP-119 immune mice or recipient mice with PfMSP-119-specific MBCs following challenge with transgenic P. berghei. Our findings suggest that PfMSP-119-specific IgG production by short-lived plasma cells combined with the poor ability of the PfMSP-119-induced MBCs to maintain the anamnestic IgG responses failed to contribute to protection against infection.
机译：裂殖子表面蛋白-1（MSP-119）的19 kDa羧基末端片段已显示出调节抗体（Ab）介导的对血液疟疾感染的保护性免疫。但是，对该抗原的血清学记忆往往是短暂的，而对于调节针对MSP-119抗原的B细胞记忆形成的机制知之甚少。我们研究了用重组19-kDa恶性疟原虫裂殖子表面蛋白1（PfMSP-119）免疫后B细胞记忆反应的形成。 PfMSP-119免疫导致生发中心（GC）B细胞数延迟增加。这种不良的GC反应与血清中PfMSP-119特异性抗体的寿命短以及脾脏和骨髓中PfMSP-119特异性浆细胞和记忆B细胞（MBC）的寿命短有关。 PfMSP-119特异的MBC能够产生抗原（Ag）特异的Ab分泌细胞（ASC）反应，该反应在用表达PfMSP-119的抗原或转基因伯氏疟原虫的原代虫替代抗原的免疫小鼠攻毒后短命上一次免疫接种后8周或过继转移到幼稚宿主后的第8周，为天然伯氏疟原虫MSP-119。但是，在用转基因伯氏疟原虫攻击后，在PfMSP-119免疫小鼠或具有PfMSP-119特异性MBC的受体小鼠中未获得保护。我们的研究结果表明，短期血浆细胞产生PfMSP-119特异性IgG以及PfMSP-119诱导的MBC维持记忆性IgG反应的能力较弱，无法帮助预防感染。

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