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首页> 外文期刊>Nature immunology >The kinase mTOR regulates the differentiation of helper T cells through the selective activation of signaling by mTORC1 and mTORC2.
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The kinase mTOR regulates the differentiation of helper T cells through the selective activation of signaling by mTORC1 and mTORC2.

机译：mTOR激酶通过mTORC1和mTORC2选择性激活信号传导来调节辅助性T细胞的分化。

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The kinase mTOR has emerged as an important regulator of the differentiation of helper T cells. Here we demonstrate that differentiation into the T(H)1 and T(H)17 subsets of helper T cells was selectively regulated by signaling from mTOR complex 1 (mTORC1) that was dependent on the small GTPase Rheb. Rheb-deficient T cells failed to generate T(H)1 and T(H)17 responses in vitro and in vivo and did not induce classical experimental autoimmune encephalomyelitis (EAE). However, they retained their ability to become T(H)2 cells. Alternatively, when mTORC2 signaling was deleted from T cells, they failed to generate T(H)2 cells in vitro and in vivo but preserved their ability to become T(H)1 and T(H)17 cells. Our data identify mechanisms by which two distinct signaling pathways downstream of mTOR regulate helper cell fate in different ways. These findings define a previously unknown paradigm that links T cell differentiation with selective metabolic signaling pathways.
机译：mTOR激酶已成为辅助性T细胞分化的重要调节剂。在这里，我们证明了通过依赖于小GTPase Rheb的mTOR复合体1（mTORC1）的信号选择性调节分化为辅助T细胞的T（H）1和T（H）17子集。 Rheb缺陷型T细胞无法在体内和体外产生T（H）1和T（H）17反应，也没有诱导经典的实验性自身免疫性脑脊髓炎（EAE）。但是，他们保留了成为T（H）2细胞的能力。或者，当从T细胞中删除mTORC2信号时，它们无法在体内和体外生成T（H）2细胞，但保留了它们成为T（H）1和T（H）17细胞的能力。我们的数据确定了mTOR下游的两个不同信号通路以不同方式调节辅助细胞命运的机制。这些发现定义了一个以前未知的范例，该范例将T细胞分化与选择性代谢信号通路联系在一起。

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