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IL-2 prevents deletion of developing T-regulatory cells in the thymus

机译:IL-2可防止缺失在胸腺中发育T-incurecatory细胞

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摘要

In the thymus, strongly self-reactive T cells may undergo apoptotic deletion or differentiate into Foxp3+ T-regulatory (T-reg) cells. Mechanisms that partition T cells into these two fates are unclear. Here, we show that IL-2 signalling is required to prevent deletion of CD4+ CD8- CCR7+ Helios+ thymocytes poised to upregulate Foxp3. The deletion prevented by IL-2 signalling is Foxp3 independent and occurs later in thymocyte development than the deletion that is prevented by Card11 signalling. Our results distinguish two bottlenecks at which strongly self-reactive thymocytes undergo deletion or progress to the next stage of T-reg differentiation; Card11 regulates the first bottleneck and IL-2 regulates the second.
机译:在胸腺中,强烈的自活性T细胞可以进行凋亡缺失或分化成FoxP3 + T-incual(T-Reg)细胞。 将T细胞分隔为这两个命令的机制尚不清楚。 在这里,我们表明IL-2信号是需要缺失CD4 + CD8-CCR7 + Helios +胸腺细胞的准备以上调Foxp3。 通过IL-2信号传导预防的缺失是Foxp3独立的,并且在胸腺细节开发后发生而不是卡11信号传导的缺失。 我们的结果区分了两种瓶颈,强烈的自活性胸腺细胞经历缺失或进展到T-Reg分化的下一阶段; CAND11规范第一个瓶颈和IL-2调节第二个瓶颈。

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  • 来源
    《Cell death and differentiation》 |2017年第6期|共10页
  • 作者单位

    Australian Natl Univ John Curtin Sch Med Res Immunol Dept Canberra ACT 0200 Australia;

    Monash Univ Monash Biomed Discovery Inst Infect &

    Immun Program Melbourne Vic 3800 Australia;

    Australian Natl Univ John Curtin Sch Med Res Immunol Dept Canberra ACT 0200 Australia;

    Australian Natl Univ John Curtin Sch Med Res Immunol Dept Canberra ACT 0200 Australia;

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  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 细胞生物学;
  • 关键词

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