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首页> 外文期刊>Immunology: An Official Journal of the British Society for Immunology >The transcriptional repressor Bcl6 controls the stability of regulatory T cells by intrinsic and extrinsic pathways
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The transcriptional repressor Bcl6 controls the stability of regulatory T cells by intrinsic and extrinsic pathways

机译：转录阻遏物Bcl6通过内在和外在途径控制调节性T细胞的稳定性

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Foxp3(+) regulatory T (Treg) cells are essential to maintain immune homeostasis, yet controversy exists about the stability of this cell population. Bcl6-deficient (Bcl6(-/-)) mice develop severe and spontaneous T helper type 2 (Th2) inflammation and Bcl6-deficient Treg cells are ineffective at controlling Th2 responses. We used a lineage tracing approach to analyse the fate of Treg cells in these mice. In the periphery of Bcl6(-/-) mice, increased numbers of Foxp3-negative exTreg' cells were found, particularly in the CD25(+) population. ExTreg cells from Bcl6(-/-) mice expressed increased interleukin-17 (IL-17) and extremely elevated levels of Th2 cytokines compared with wild-type exTreg cells. Although Treg cells normally express only low levels of cytokines, Treg cells from Bcl6(-/-) mice secreted higher levels of IL-4, IL-5, IL-13 and IL-17 than wild-type conventional T cells. Next, Treg-specific conditional Bcl6-deficient (Bcl6(Foxp3-/-)) mice were analysed. Bcl6(Foxp3-/-) mice do not develop inflammatory disease, indicating a requirement for non-Treg cells for inflammation in Bcl6(-/-) mice, and have normal numbers of exTreg cells. We induced Th2-type allergic airway inflammation in Bcl6(Foxp3-/-) mice, and found that while exTreg cytokine expression was normal, Bcl6-deficient Treg cells expressed higher levels of the Th2-specific regulator Gata3 than Bcl6(+) Treg cells. Bcl6(Foxp3-/-) mice had increased numbers of Th2 cells after induction of airway inflammation and increased T cells in the bronchoalveolar lavage fluid. These data show both Treg-intrinsic and Treg-extrinsic roles for Bcl6 in controlling Treg cell stability and Th2 inflammation, and support the idea that Bcl6 expression in Treg cells is critical for controlling Th2 responses.
机译：Foxp3（+）调节性T（Treg）细胞对于维持免疫稳态是必不可少的，但是关于该细胞群体的稳定性存在争议。缺乏Bcl6的（Bcl6（-/-））小鼠发生严重和自发的2型辅助性T辅助炎症（Th2），缺乏Bcl6的Treg细胞不能有效控制Th2反应。我们使用谱系追踪方法来分析这些小鼠中Treg细胞的命运。在Bcl6（-/-）小鼠的外围，发现增加的Foxp3阴性exTreg'细胞数量增加，特别是在CD25（+）群体中。与野生型exTreg细胞相比，来自Bcl6（-/-）小鼠的ExTreg细胞表达的白介素17（IL-17）升高，Th2细胞因子水平极高。尽管Treg细胞通常仅表达低水平的细胞因子，但与野生型常规T细胞相比，来自Bcl6（-/-）小鼠的Treg细胞分泌更高水平的IL-4，IL-5，IL-13和IL-17。接下来，分析Treg特异性的条件性Bcl6-缺陷（Bcl6（Foxp3-/-））小鼠。 Bcl6（Foxp3-/-）小鼠没有发生炎症性疾病，表明需要非Treg细胞用于Bcl6（-/-）小鼠的炎症，并且具有正常数量的exTreg细胞。我们在Bcl6（Foxp3-/-）小鼠中诱导了Th2型过敏性气道炎症，发现exTreg细胞因子表达正常，而Bcl6缺陷型Treg细胞表达的Th2特异性调节剂Gata3的水平高于Bcl6（+）Treg细胞。 。 Bcl6（Foxp3-/-）小鼠诱导气道炎症后，Th2细胞数量增加，支气管肺泡灌洗液中的T细胞数量增加。这些数据显示了Bcl6在控制Treg细胞稳定性和Th2炎症中的Treg内在和Treg外在作用，并支持Treg细胞中Bcl6表达对于控制Th2反应至关重要的观点。

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