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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Induction of CD4~+CD25~+ regulatory T cells by copolymer-Ⅰ through activation of transcription factor Foxp3
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Induction of CD4~+CD25~+ regulatory T cells by copolymer-Ⅰ through activation of transcription factor Foxp3

机译：活化转录因子Foxp3通过共聚物Ⅰ诱导CD4〜+ CD25〜+调节性T细胞

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摘要

Copolymer-Ⅰ (COP-Ⅰ) has unique immune regulatory properties and is a treatment option for multiple sclerosis (MS). This study revealed that COP-Ⅰ induced the conversion of peripheral CD4~+CD25~+ to CD4~+CD25~+ regulatory T cells through the activation of transcription factor Foxp3. COP-Ⅰ treatment led to a significant increase in Foxp3 expression in CD4~+ T cells in MS patients whose Foxp3 expression was reduced at baseline. CD4~+CD25~+ T cell lines generated by COP-Ⅰ expressed high levels of Foxp3 that correlated with an increased regulatory potential. Furthermore, we demonstrated that the induction of Foxp3 in CD4~+ T cells by COP-Ⅰ was mediated through its ability to produce IFN-γ and, to a lesser degree, TGF-β1, as shown by antibody blocking and direct cytokine induction of Foxp3 expression in T cells. It was evident that in vitro treatment and administration with COP-Ⅰ significantly raised the level of Foxp3 expression in CD4~+ T cells and promoted conversion of CD4~+CD25~+ regulatory T cells in wild-type B6 mice but not in IFN-γ knockout mice. This study provides evidence for the role and mechanism of action of COP-Ⅰ in the induction of CD4~+CD25~+ regulatory T cells in general and its relevance to the treatment of MS.
机译：共聚物-Ⅰ（COP-Ⅰ）具有独特的免疫调节特性，是多发性硬化症（MS）的治疗选择。这项研究表明，COP-Ⅰ通过激活转录因子Foxp3诱导外周CD4〜+ CD25〜+向CD4〜+ CD25〜+调节性T细胞的转化。 COP-Ⅰ治疗导致基线时Foxp3表达降低的MS患者CD4〜+ T细胞中Foxp3表达显着增加。 COP-Ⅰ产生的CD4〜+ CD25〜+ T细胞系表达高水平的Foxp3，与调节潜能增加有关。此外，我们证明了COP-Ⅰ诱导CD4〜+ T细胞中Foxp3的诱导是通过其产生IFN-γ的能力介导的，在较小程度上是TGF-β1的能力，如抗体的阻断和细胞因子的直接诱导所显示的那样。 Foxp3在T细胞中的表达。显然，在体外处理和施用COP-Ⅰ可以显着提高野生型B6小鼠CD4〜+ T细胞中Foxp3表达的水平，并促进CD4〜+ CD25〜+调节性T细胞的转化，而在IFN-γ中则没有。 γ基因敲除小鼠。这项研究为COP-Ⅰ在诱导CD4〜+ CD25〜+调节性T细胞中的作用和作用机理提供了证据，并与MS的治疗有关。

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