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首页> 外文期刊>Parasitology >Effects of CD4(+)CD25(+)Foxp3(+)regulatory T cells on early Plasmodium yoelii 17XL infection in BALB/c mice.
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Effects of CD4(+)CD25(+)Foxp3(+)regulatory T cells on early Plasmodium yoelii 17XL infection in BALB/c mice.

机译：CD4（+）CD25（+）Foxp3（+）调节性T细胞对BALB / c小鼠早期约氏疟原虫17XL感染的影响。

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摘要

The outcome of Plasmodium yoelii 17XL-infected BALB/c and DBA/2 mice, ranging from death to spontaneous cure, respectively, depends largely on the establishment of effective pro-inflammatory type 1 responses during the early stages of infection and associates with CD4(+)CD25(+)Foxp3(+)regulatory T cells (Tregs). Here, effects of Tregs were analysed on early P. yoelii 17XL infection in BALB/c and DBA/2 mice. In vivo depletion of Tregs significantly reversed the inhibited establishment of effective pro-inflammatory type 1 responses in BALB/c mice, indicating that this cell population contributed to the suppression of T-cell function in malaria. Moreover, the proportion and absolute numbers of IL-10-secreting Tregs in BALB/c mice were significantly higher than that found in DBA/2 mice by intracytoplasmic staining, and IL-10 production was correlated with the Tregs population. In addition, in vivo Tregs depletion decreased the production of IL-10 and the apoptosis of CD4+ T cells. Consistently, IL-10R blockade also had the same effect as that of Tregs depletion in P. yoelii 17XL-infected BALB/c mice. Our data demonstrate that Tregs perhaps have an important role in regulating pro-inflammatory type 1 responses in an IL-10-dependent manner and induce CD4+ T cell apoptosis during the early stage of P. yoelii 17XL infection.
机译：从死亡到自发治愈的分别受约氏疟原虫17XL感染的BALB / c和DBA / 2小鼠的结果在很大程度上取决于感染早期阶段有效的促炎1型反应的建立，并与CD4相关（ +）CD25（+）Foxp3（+）调节性T细胞（Tregs）。在这里，分析了Tregs对BALB / c和DBA / 2小鼠早期约氏疟原虫17XL感染的影响。 Tregs的体内耗竭显着逆转了BALB / c小鼠中有效促炎1型应答的抑制建立，表明该细胞群有助于抑制T细胞在疟疾中的功能。此外，通过细胞质内染色，BALB / c小鼠中分泌IL-10的Treg的比例和绝对数量显着高于DBA / 2小鼠，并且IL-10的产生与Tregs群体有关。另外，体内Tregs的消耗降低了IL-10的产生和CD4 + T细胞的凋亡。一致地，IL-10R阻断作用与感染约氏疟原虫17XL感染的BALB / c小鼠的Treg耗竭相同。我们的数据表明，Tregs可能在依赖IL-10的方式调节促炎1型应答中起重要作用，并在约氏疟原虫17XL感染的早期诱导CD4 + T细胞凋亡。

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