当前位置: X-MOL 学术Microbiol. Immunol. › 论文详情
Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)
Plasmodium infection cure cycles induce modulation of conventional dendritic cells.
Microbiology and Immunology ( IF 2.6 ) Pub Date : 2020-02-25 , DOI: 10.1111/1348-0421.12783
Ryosuke Adachi 1 , Takahiko Tamura 1
Affiliation  

Malaria is one of the most widespread human infectious diseases worldwide and a cause of mortality. It is difficult to induce immunological memory against the malarial parasite Plasmodium . The immunity to clinical malaria disease is acquired with multiple infection and treatment cycles, along with substantial reduction in parasite burden. However, the mechanism of the acquired immunity remains largely unclear. Conventional DCs (cDCs) play a pivotal role in orchestration of immune responses. The purpose of this study is to analyze the characterization of cDCs after the infection and cure treatment cycles. Mice were infected with the lethal rodent malarial parasite Plasmodium berghei ANKA, which was followed by cure treatment with the antimalarial drug pyrimethamine. This was then followed by a challenge with live parasites. The mice that went through infection cure cycles showed significant immune response, demonstrating robust immunological memory against malaria parasites. We investigated the cytokine production capacity of splenic cDCs in both naive and infection cure mice by stimulating purified splenic cDCs with LPS (TLR4 agonist) or CpG (TLR9 agonist). The capacity of cytokine production was found to be significantly decreased in infection cure mice. The suppression of cytokine production was sustained for a long term (6 months). Moreover, the surface expression of MHC Class II molecules was significantly lower in infection cure mice than in naive mice. These results suggest that Plasmodium infection and cure treatment resulted in strong immunological memory and modulation of full functionality of cDCs.

中文翻译:

疟原虫感染的治愈周期诱导常规树突状细胞的调节。

疟疾是全世界最广泛的人类传染病之一,也是造成死亡的原因。很难诱导针对疟原虫疟原虫的免疫记忆。通过多个感染和治疗周期以及大量减少寄生虫负担,可以获得对临床疟疾疾病的免疫力。但是,获得性免疫的机制在很大程度上仍不清楚。常规DC(cDC)在协调免疫反应中起着关键作用。这项研究的目的是分析感染和治愈治疗周期后cDC的特征。小鼠感染了致命的啮齿类疟疾寄生虫伯氏疟原虫ANKA,然后用抗疟药乙胺嘧啶进行治愈。然后是活寄生虫的挑战。经历感染治愈周期的小鼠表现出明显的免疫反应,表现出针对疟原虫的强大免疫记忆。我们通过用LPS(TLR4激动剂)或CpG(TLR9激动剂)刺激纯化的脾脏cDC,研究了幼稚和感染治愈小鼠中脾脏cDC的细胞因子生产能力。发现感染治愈小鼠中细胞因子产生的能力显着降低。细胞因子产生的抑制作用持续了很长时间(6个月)。而且,感染治愈小鼠中的MHC II类分子的表面表达明显低于幼稚小鼠。这些结果表明,疟原虫 感染和治愈治疗导致强大的免疫记忆和cDC完整功能的调节。
更新日期:2020-02-25
down
wechat
bug