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首页> 外文期刊>Infection and immunity >CD4+ CD25+ Foxp3+ Regulatory T Cells, Dendritic Cells, and Circulating Cytokines in Uncomplicated Malaria: Do Different Parasite Species Elicit Similar Host Responses?
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CD4+ CD25+ Foxp3+ Regulatory T Cells, Dendritic Cells, and Circulating Cytokines in Uncomplicated Malaria: Do Different Parasite Species Elicit Similar Host Responses?

机译：单纯性疟疾中的CD4 + CD25 + Foxp3 +调节性T细胞，树突状细胞和循环细胞因子：不同的寄生虫物种引起类似的宿主反应吗？

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Clearing blood-stage malaria parasites without inducing major host pathology requires a finely tuned balance between pro- and anti-inflammatory responses. The interplay between regulatory T (Treg) cells and dendritic cells (DCs) is one of the key determinants of this balance. Although experimental models have revealed various patterns of Treg cell expansion, DC maturation, and cytokine production according to the infecting malaria parasite species, no studies have compared all of these parameters in human infections with Plasmodium falciparum and P. vivax in the same setting of endemicity. Here we show that during uncomplicated acute malaria, both species induced a significant expansion of CD4+ CD25+ Foxp3+ Treg cells expressing the key immunomodulatory molecule CTLA-4 and a significant increase in the proportion of DCs that were plasmacytoid (CD123+), with a decrease in the myeloid/plasmacytoid DC ratio. These changes were proportional to parasite loads but correlated neither with the intensity of clinical symptoms nor with circulating cytokine levels. One-third of P. vivax-infected patients, but no P. falciparum-infected subjects, showed impaired maturation of circulating DCs, with low surface expression of CD86. Although vivax malaria patients overall had a less inflammatory cytokine response, with a higher interleukin-10 (IL-10)/tumor necrosis factor alpha (TNF-α) ratio, this finding did not translate to milder clinical manifestations than those of falciparum malaria patients. We discuss the potential implications of these findings for species-specific pathogenesis and long-lasting protective immunity to malaria.
机译：在不引起主要宿主病理的情况下清除血液阶段的疟疾寄生虫需要在促炎和抗炎反应之间进行微调。调节性T（Treg）细胞与树突状细胞（DC）之间的相互作用是这种平衡的关键决定因素之一。尽管实验模型根据感染的疟原虫种类揭示了Treg细胞扩增，DC成熟和细胞因子产生的各种模式，但尚无研究将人感染恶性疟原虫和em的所有这些参数进行比较。 > P。 vivax 在相同的地方流行。在这里，我们表明在简单的急性疟疾中，两种物种均诱导表达关键免疫调节分子的CD4 + CD25 + Foxp3 + Treg细胞显着扩增CTLA-4和浆细胞样DC（CD123 + ）的DC比例显着增加，而髓样/浆细胞样DC比率降低。这些变化与寄生虫负荷成正比，但与临床症状的强度或循环细胞因子水平均无关。 P的三分之一。间质感染的患者，但没有 P。恶性疟原虫感染的受试者表现出循环DC的成熟受损，CD86的表面表达较低。尽管间日间疟原虫患者的炎症细胞因子反应总体较少，白介素10（IL-10）/肿瘤坏死因子α（TNF-α）比率较高，但这一发现并没有比恶性疟原虫患者更轻的临床表现。我们讨论这些发现对物种特异性发病机制和对疟疾的长期保护性免疫的潜在影响。

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