Plasmodium parasite-specific antibodies are critical for protection against malaria, yet the development of long-lived and effective humoral immunity against Plasmodium takes many years and multiple rounds of infection and cure. Here, we report that the rapid development of short-lived plasmablasts during experimental malaria unexpectedly hindered parasite control by impeding germinal center responses. Metabolic hyperactivity of plasmablasts resulted in nutrient deprivation of the germinal center reaction, limiting the generation of memory B cell and long-lived plasma cell responses. Therapeutic administration of a single amino acid to experimentally infected mice was sufficient to overcome the metabolic constraints imposed by plasmablasts and enhanced parasite clearance and the formation of protective humoral immune memory responses. Thus, our studies not only challenge the current model describing the role and function of blood-stage Plasmodium-induced plasmablasts but they also reveal new targets and strategies to improve anti-Plasmodium humoral immunity.

中文翻译：

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感染引起的成浆细胞是一种营养库，会削弱体液对疟疾的免疫力。

疟原虫寄生虫特异性抗体对于预防疟疾至关重要，但是针对疟原虫的长期有效的体液免疫的发展需要很多年，并且需要多轮感染和治愈。在这里，我们报告说，实验性疟疾期间短寿命成浆细胞的快速发展出乎意料地通过阻碍生发中心反应而阻碍了寄生虫的控制。成浆细胞的代谢亢进导致生发中心反应的营养缺乏，从而限制了记忆B细胞的生成和长寿的浆细胞反应。对实验感染的小鼠进行单一氨基酸的治疗性给药足以克服由成浆细胞和增强的寄生虫清除以及保护性体液免疫记忆反应的形成所引起的代谢限制。从而，