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首页> 外文期刊>Cell Research >Downregulation of CD4+CD25+ regulatory T cells may underlie enhanced Th1 immunity caused by immunization with activated autologous T cells
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Downregulation of CD4+CD25+ regulatory T cells may underlie enhanced Th1 immunity caused by immunization with activated autologous T cells

机译：CD4 + CD25 +调节性T细胞的下调可能是由活化的自体T细胞免疫引起的增强的Th1免疫力的基础

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Regulatory T cells (Treg) play important roles in immune system homeostasis, and may also be involved in tumor immunotolerance by suppressing Thl immune response which is involved in anti-tumor immunity. We have previously reported that immunization with attenuated activated autologous T cells leads to enhanced anti-tumor immunity and upregulated Thl responses in vivo. However, the underlying molecular mechanisms are not well understood. Here we show that Treg function was significantly downregulated in mice that received immunization of attenuated activated autologous T cells. We found that Foxp3 expression decreased in CD4+CD25+ T cells from the immunized mice. Moreover, CD4+CD25+Foxp3+ Treg obtained from immunized mice exhibited diminished immunosuppression ability compared to those from naive mice. Further analysis showed that the serum of immunized mice contains a high level of anti-CD25 antibody (about 30 ng/ml, p < 0.01 vs controls). Consistent with a role of anti-CD25 response in the down-regulation of Treg, adoptive transfer of serum from immunized mice to naive mice led to a significant decrease in Treg population and function in recipient mice. The triggering of anti-CD25 response in immunized mice can be explained by the fact that CD25 was induced to a high level in the ConA activated autologous T cells used for immunization. Our results demonstrate for the first time that immunization with attenuated activated autologous T cells evokes anti-CD25 antibody production, which leads to impeded CD4+CD25+Foxp3+ Treg expansion and function in vivo. We suggest that dampened Treg function likely contributes to enhanced Thl response in immunized mice and is at least part of the mechanism underlying the boosted anti-tumor immunity.
机译：调节性T细胞（Treg）在免疫系统稳态中起重要作用，并且还可以通过抑制与抗肿瘤免疫有关的Th1免疫应答来参与肿瘤的免疫耐受。我们以前曾报道过，用减毒的活化自体T细胞免疫会增强体内的抗肿瘤免疫力和Th1反应。然而，潜在的分子机制还没有被很好地理解。在这里，我们显示在接受减毒激活的自体T细胞免疫的小鼠中，Treg功能显着下调。我们发现，Foxp3表达在来自免疫小鼠的CD4 + CD25 + T细胞中下降。此外，从免疫小鼠获得的CD4 + CD25 + Foxp3 + Treg与从幼稚小鼠获得的免疫抑制能力相比降低。进一步的分析表明，免疫小鼠的血清中含有高水平的抗CD25抗体（约30 ng / ml，与对照组相比，p <0.01）。与抗CD25反应在Treg的下调中的作用一致，过继地将血清从免疫小鼠转移至幼稚小鼠导致Treg种群和受体小鼠功能的显着降低。免疫小鼠中抗CD25应答的触发可以通过以下事实来解释：在用于免疫的ConA激活的自体T细胞中CD25诱导水平很高。我们的结果首次证明，用减毒的活化自体T细胞免疫可激发抗CD25抗体的产生，从而导致CD4 + CD25 + Foxp3 + Treg的扩增和体内功能受到阻碍。我们建议减弱的Treg功能可能有助于在免疫小鼠中增强Thl反应，并且至少是增强的抗肿瘤免疫基础的一部分。

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