Transcription factor interplay in T helper cell differentiation.

Transcription factor interplay in T helper cell differentiation.
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DOI:
10.1093/bfgp/elt025
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发表时间:
2013-11
影响因子:
4
通讯作者:
Jenner RG
Jenner RG
中科院分区:
生物学3区
文献类型:
--
作者:
Evans CM;Jenner RG

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CD 4辅助性T细胞分化为特化效应细胞谱系为理解免疫细胞分化提供了一个强有力的模型。不同的谱系已被定义的差异表达的签名细胞因子和谱系特异性转录因子的必要和足够的生产。分别由T-bet和GATA 3驱动的向Th 1和Th 2亚型分化的传统范例已经扩展到并入额外的T细胞谱系和转录调节因子。技术进步已经将我们对这些谱系特异性转录因子的看法扩展到整个基因组,并揭示了它们之间意想不到的相互作用。从这些数据来看,血统规范比以前的模型所暗示的更加复杂和可塑。在这里,我们提出了一个概述的不同形式的转录因子的相互作用,已被确定和T细胞表型如何出现这种相互作用的产物在复杂的调控网络。我们还建议实验策略,将提供进一步深入了解的机制,T细胞谱系规范和可塑性。
The differentiation of CD4 helper T cells into specialized effector lineages has provided a powerful model for understanding immune cell differentiation. Distinct lineages have been defined by differential expression of signature cytokines and the lineage-specifying transcription factors necessary and sufficient for their production. The traditional paradigm of differentiation towards Th1 and Th2 subtypes driven by T-bet and GATA3, respectively, has been extended to incorporate additional T cell lineages and transcriptional regulators. Technological advances have expanded our view of these lineage-specifying transcription factors to the whole genome and revealed unexpected interplay between them. From these data, it is becoming clear that lineage specification is more complex and plastic than previous models might have suggested. Here, we present an overview of the different forms of transcription factor interplay that have been identified and how T cell phenotypes arise as a product of this interplay within complex regulatory networks. We also suggest experimental strategies that will provide further insight into the mechanisms that underlie T cell lineage specification and plasticity.
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