Naito Taku, Muroi Sawako, Taniuchi Ichiro, Kondo Motonari
Department of Molecular Immunology, Toho University School of Medicine, Tokyo, Japan.
Laboratory for Gene Regulation, Institute for Medical Sciences, RIKEN, Yokohama, Japan.
Data Brief. 2018 Feb 17;17:1180-1183. doi: 10.1016/j.dib.2018.02.045. eCollection 2018 Apr.
The data presented here are related to the research article entitled "Loss of Eed leads to lineage instability and increased CD8 expression of mouse CD4 T cells upon TGFβ signaling" [1]. The cited research article investigates the molecular mechanism of CD8α upregulation observed in -deficient () CD4 T cells upon activation in the presence of TGFβ. This data report describes the effect of retinoic acid (RA) and/or anti-interferon-gamma (IFNγ) antibody supplementation on up-regulation of CD8α and Foxp3 in CD4 T cells, the effect of dose or timing of TGFβ treatment on CD4 T cell identity of , adding further information regarding the conditions that induces CD8α, and mRNA expression changes of genes encoding polycomb repressive complex 2 (PRC2) subunits by TGFβ treatment.
此处呈现的数据与题为《Eed缺失导致TGFβ信号传导时小鼠CD4 T细胞谱系不稳定及CD8表达增加》的研究文章[1]相关。引用的研究文章探究了在TGFβ存在的情况下激活时，在Eed缺陷（Eed -/-）CD4 T细胞中观察到的CD8α上调的分子机制。本数据报告描述了视黄酸（RA）和/或抗干扰素-γ（IFNγ）抗体补充对Eed -/- CD4 T细胞中CD8α和Foxp3上调的影响，TGFβ处理的剂量或时间对Eed -/- CD4 T细胞特性的影响，补充了关于诱导CD8α的条件的更多信息，以及TGFβ处理对编码多梳抑制复合物2（PRC2）亚基的基因的mRNA表达变化。
