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Transcription factor Foxp1 regulates Foxp3 chromatin binding and coordinates regulatory T cell function.
Nature Immunology ( IF 27.7 ) Pub Date : 2019-01-14 , DOI: 10.1038/s41590-018-0291-z
Catherine Konopacki 1, 2 , Yuri Pritykin 3 , Yury Rubtsov 4, 5 , Christina S Leslie 3 , Alexander Y Rudensky 1, 2, 6
Nature Immunology ( IF 27.7 ) Pub Date : 2019-01-14 , DOI: 10.1038/s41590-018-0291-z
Catherine Konopacki 1, 2 , Yuri Pritykin 3 , Yury Rubtsov 4, 5 , Christina S Leslie 3 , Alexander Y Rudensky 1, 2, 6
Affiliation
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Regulatory T cells (Treg cells), whose differentiation and function are controlled by transcription factor Foxp3, express the closely related family member Foxp1. Here we explored Foxp1 function in Treg cells. We found that a large number of Foxp3-bound genomic sites in Treg cells were occupied by Foxp1 in both Treg cells and conventional T cells (Tconv cells). In Treg cells, Foxp1 markedly increased Foxp3 binding to these sites. Foxp1 deficiency in Treg cells resulted in their impaired function and competitive fitness, associated with markedly reduced CD25 expression and interleukin-2 (IL-2) responsiveness, diminished CTLA-4 expression and increased SATB1 expression. The characteristic expression patterns of CD25, Foxp3 and CTLA-4 in Treg cells were fully or partially rescued by strong IL-2 signaling. Our studies suggest that Foxp1 serves an essential non-redundant function in Treg cells by enforcing Foxp3-mediated regulation of gene expression and enabling efficient IL-2 signaling in these cells.
中文翻译：
转录因子Foxp1调节Foxp3染色质结合并协调调节性T细胞功能。
调节性T细胞（Treg细胞）的分化和功能受转录因子Foxp3的控制，它表达密切相关的家族成员Foxp1。在这里，我们探讨了Treg细胞中Foxp1的功能。我们发现，Treg细胞和常规T细胞（Tconv细胞）中的Foxp1占据了Treg细胞中大量Foxp3结合的基因组位点。在Treg细胞中，Foxp1明显增加了Foxp3与这些位点的结合。Treg细胞中的Foxp1缺乏症导致其功能和竞争能力受损，与CD25表达和白介素2（IL-2）应答性显着降低，CTLA-4表达减少以及SATB1表达增加有关。Treg细胞中CD25，Foxp3和CTLA-4的特征性表达模式可通过强力的IL-2信号完全或部分挽救。
更新日期：2019-01-25
中文翻译：
转录因子Foxp1调节Foxp3染色质结合并协调调节性T细胞功能。
调节性T细胞（Treg细胞）的分化和功能受转录因子Foxp3的控制，它表达密切相关的家族成员Foxp1。在这里，我们探讨了Treg细胞中Foxp1的功能。我们发现，Treg细胞和常规T细胞（Tconv细胞）中的Foxp1占据了Treg细胞中大量Foxp3结合的基因组位点。在Treg细胞中，Foxp1明显增加了Foxp3与这些位点的结合。Treg细胞中的Foxp1缺乏症导致其功能和竞争能力受损，与CD25表达和白介素2（IL-2）应答性显着降低，CTLA-4表达减少以及SATB1表达增加有关。Treg细胞中CD25，Foxp3和CTLA-4的特征性表达模式可通过强力的IL-2信号完全或部分挽救。
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