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

机译:IL-2可防止胸腺中发育的T调节细胞的缺失

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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,强烈自我反应的T细胞可能会发生凋亡缺失或分化为Foxp3 + T调节(T-reg)细胞。将T细胞分为这两种命运的机制尚不清楚。在这里,我们表明需要IL-2信号来防止CD4 + CD8–CCR7 + Helios +胸腺细胞的缺失,从而上调Foxp3。 IL-2信号传导阻止的缺失是Foxp3独立的,并且在胸腺细胞发育中的发生比Card11信号传导阻止的缺失晚。我们的结果区分了两个瓶颈,在这两个瓶颈处,强烈自我反应的胸腺细胞经历缺失或进入T-reg分化的下一阶段。 Card11调节第一个瓶颈,IL-2调节第二个瓶颈。

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