Though the immunity to malaria has been associated with cellular immune responses, the exact function of the phenotypic cell population is still unclear. This study investigated the host immune responses elicited during the pre-erythrocytic stage, post-Plasmodium yoelii sporozoite infection in Swiss mice model. For this purpose, we analyzed the dynamics of different subsets of immune cells population and cytokine levels in the hepatic mononuclear and splenic cells population during pre-erythrocytic liver-stage infection. We observed a significant reduction in the effectors immune cells population including CD8⁺ T cell, F4/80⁺ macrophage and in plasmacytoid dendritic cells (CD11c⁺ B220⁺). Interestingly, substantial down-regulation was also noted in pro-inflammatory cytokines (i.e. IFN-γ, TNF-α, IL-12, IL-2, IL-17 and iNOS), while, up-regulation of anti-inflammatory cytokines (i.e. IL-10, IL-4 and TGF-β) during asymptomatic pre-erythrocytic liver-stage infection. Collectively, this study demonstrated that during pre-erythrocytic development, Plasmodium yoelii sporozoite impaired the host activators of innate and adaptive immune responses by regulating the immune effector cells, gene expression and cytokines levels for the establishment of infection and subsequent development in the liver and spleen. The results in this study provided a better understanding of the events leading to malarial infection and will be helpful in supportive treatment and vaccine development strategy.

尽管对疟疾的免疫与细胞免疫反应有关，但表型细胞群的确切功能仍不清楚。这项研究调查了瑞士小鼠模型在红细胞生成前阶段，约氏疟原虫子孢子感染后引发的宿主免疫反应。为此，我们分析了在红细胞前期肝阶段感染过程中，肝细胞单个核和脾细胞群中免疫细胞群和细胞因子水平的不同亚群的动态。我们观察到效应免疫细胞（包括CD8 ⁺ T细胞，F4 / 80 ⁺巨噬细胞）和浆细胞样树突状细胞（CD11c ⁺ B220 ⁺）。有趣的是，促炎细胞因子（即IFN-γ，TNF-α，IL-12，IL-2，IL-17和iNOS）也出现了明显的下调，而抗炎细胞因子（在无症状的前红细胞肝期感染期间，即IL-10，IL-4和TGF-β）。总体而言，这项研究表明，在红细胞形成前，约氏疟原虫子孢子通过调节免疫效应细胞，基因表达和细胞因子水平来损害感染的建立以及随后在肝脏和脾脏的发育中损害先天性和适应性免疫应答的宿主激活剂。 。这项研究的结果更好地理解了导致疟疾感染的事件，将有助于支持治疗和疫苗开发策略。