Burnet Institute, Melbourne, VIC, Australia.
Department of Medicine, The University of Melbourne, Parkville, VIC, Australia.
Front Immunol. 2019 Jan 31;10:32. doi: 10.3389/fimmu.2019.00032. eCollection 2019.
Dendritic cells are key linkers of innate and adaptive immunity. Efficient dendritic cell activation is central to the acquisition of immunity and the efficacy of vaccines. Understanding how dendritic cells are affected by blood-stage parasites will help to understand how immunity is acquired and maintained, and how vaccine responses may be impacted by malaria infection or exposure. This study investigates the response of dendritic cells to two different life stages of the malaria parasite, parasitized red blood cells and merozoites, using a murine model. We demonstrate that the dendritic cell responses to merozoites are robust whereas dendritic cell activation, particularly CD40 and pro-inflammatory cytokine expression, is compromised in the presence of freshly isolated parasitized red blood cells. The mechanism of dendritic cell suppression by parasitized red blood cells is host red cell membrane-independent. Furthermore, we show that cryopreserved parasitized red blood cells have a substantially reduced capacity for dendritic cell activation.
树突状细胞是先天免疫和适应性免疫的关键连接者。有效的树突状细胞激活对于获得免疫和疫苗的效果至关重要。了解血液阶段寄生虫如何影响树突状细胞将有助于理解免疫是如何获得和维持的，以及疟疾感染或暴露如何影响疫苗反应。本研究使用鼠模型研究了树突状细胞对疟原虫两种不同生活阶段（寄生红细胞和裂殖子）的反应。我们证明，裂殖子对树突状细胞的反应是强烈的，而在新鲜分离的寄生红细胞存在的情况下，树突状细胞的激活，特别是 CD40 和促炎细胞因子的表达，受到损害。寄生红细胞抑制树突状细胞的机制与宿主红细胞膜无关。此外，我们还表明，冷冻保存的寄生红细胞激活树突状细胞的能力大大降低。
