Eomesodermin 促进 RelA 和 NFATc2 与小鼠淋巴瘤 BW5147 细胞中 Ifng 启动子和多个 Ifng 基因座保守非编码序列的相互作用。
Eomesodermin promotes interaction of RelA and NFATc2 with the Ifng promoter and multiple conserved noncoding sequences across the Ifng locus in mouse lymphoma BW5147 cells.
机构信息
Department of Applied Biology, Kyoto Institute of Technology, Matsugasaki, Sakyo-ku, Kyoto, 606-8585, Japan.
Department of Applied Biology, Kyoto Institute of Technology, Matsugasaki, Sakyo-ku, Kyoto, 606-8585, Japan; The Center for Advanced Insect Research Promotion (CAIRP), Kyoto Institute of Technology, Matsugasaki, Sakyo-ku, Kyoto, 606-8585, Japan.
出版信息
Immunol Lett. 2020 Sep;225:33-43. doi: 10.1016/j.imlet.2020.06.008. Epub 2020 Jun 15.
The T-box transcription factor Eomesodermin (Eomes) regulates the lineage-dependent expression of interferon γ (IFN-γ). We previously showed that Eomes promotes IFN-γ production and interacts with multiple conserved noncoding sequences (CNS) across the Ifng locus in mouse lymphoma BW5147 cells. In the present study, we investigated the transcriptional regulation of IFN-γ by the nuclear factor κB (NF-κB) subunit RelA and nuclear factor of activated T cells c2 (NFATc2, also known as NFAT1) in Eomes-transfected BW5147 cells. Eomes promoted the interaction of RelA and NFATc2 with the Ifng promoter and five CNS, including CNS-22 and CNS+30 upon stimulation with phorbol 12-myristate 13-acetate (PMA) and ionomycin (IM). The dual NF-κB and STAT3 inhibitor TPCA-1 moderately reduced the PMA- and IM-induced IFN-γ transcription in Eomes-transfected BW5147 cells. TPCA-1 interfered with RelA binding to the Ifng promoter, CNS-22 and CNS+30. Moreover, TPCA-1 reduced the interaction of Eomes or NFATc2 with the Ifng promoter and CNS+30. The present results indicate that Eomes promotes the interaction of RelA and NFATc2 with the Ifng promoter and multiple CNS across the Ifng locus in BW5147 cells.
T 盒转录因子 Eomesodermin（Eomes）调节干扰素 γ（IFN-γ）的谱系依赖性表达。我们之前表明，Eomes 促进 IFN-γ 的产生，并与小鼠淋巴瘤 BW5147 细胞中 Ifng 基因座上的多个保守非编码序列（CNS）相互作用。在本研究中，我们研究了核因子 κB（NF-κB）亚基 RelA 和激活的 T 细胞核因子 c2（NFATc2，也称为 NFAT1）在 Eomes 转染的 BW5147 细胞中对 IFN-γ 的转录调控。Eomes 促进了 RelA 和 NFATc2 与 Ifng 启动子和五个 CNS（包括 CNS-22 和 CNS+30）的相互作用，在佛波醇 12-肉豆蔻酸 13-乙酸酯（PMA）和离子霉素（IM）刺激下。双重 NF-κB 和 STAT3 抑制剂 TPCA-1 适度降低了 Eomes 转染的 BW5147 细胞中 PMA 和 IM 诱导的 IFN-γ 转录。TPCA-1 干扰了 RelA 与 Ifng 启动子、CNS-22 和 CNS+30 的结合。此外，TPCA-1 降低了 Eomes 或 NFATc2 与 Ifng 启动子和 CNS+30 的相互作用。本研究结果表明，Eomes 促进了 RelA 和 NFATc2 与 BW5147 细胞中 Ifng 基因座上的 Ifng 启动子和多个 CNS 的相互作用。
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