Department of Internal Medicine, Yale School of Medicine, New Haven, CT, 06520, USA.
Department of Pathology, Yale School of Medicine, New Haven, CT, 06520, USA.
Nat Commun. 2018 Jul 13;9(1):2714. doi: 10.1038/s41467-018-05041-7.
Plasmodium species produce an ortholog of the cytokine macrophage migration inhibitory factor, PMIF, which modulates the host inflammatory response to malaria. Using a novel RNA replicon-based vaccine, we show the impact of PMIF immunoneutralization on the host response and observed improved control of liver and blood-stage Plasmodium infection, and complete protection from re-infection. Vaccination against PMIF delayed blood-stage patency after sporozoite infection, reduced the expression of the Th1-associated inflammatory markers TNF-α, IL-12, and IFN-γ during blood-stage infection, augmented Tfh cell and germinal center responses, increased anti-Plasmodium antibody titers, and enhanced the differentiation of antigen-experienced memory CD4 T cells and liver-resident CD8 T cells. Protection from re-infection was recapitulated by the adoptive transfer of CD8 or CD4 T cells from PMIF RNA immunized hosts. Parasite MIF inhibition may be a useful approach to promote immunity to Plasmodium and potentially other parasite genera that produce MIF orthologous proteins.
疟原虫产生细胞因子巨噬细胞移动抑制因子(MIF)的同源物 PMIF,它调节宿主对疟疾的炎症反应。我们使用一种新的基于 RNA 复制子的疫苗,研究了 PMIF 免疫中和对宿主反应的影响,观察到对肝脏和血液阶段疟原虫感染的控制得到改善,并完全防止了再感染。针对 PMIF 的疫苗接种可延迟疟原虫感染后血期的出现,减少血期感染时与 Th1 相关的炎症标志物 TNF-α、IL-12 和 IFN-γ的表达,增强滤泡辅助性 T 细胞(Tfh)和生发中心反应,增加抗疟原虫抗体滴度,并增强抗原经历的记忆 CD4 T 细胞和肝驻留 CD8 T 细胞的分化。从 PMIF RNA 免疫接种的宿主中过继转移 CD8 或 CD4 T 细胞可重现对再感染的保护。寄生虫 MIF 抑制可能是促进对疟原虫和潜在其他产生 MIF 同源蛋白的寄生虫属免疫的一种有用方法。