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Updated: Feb 3, 2026

In Vitro Differentiation of Human CD4+FOXP3+ Induced Regulatory T Cells (iTregs) from Naïve CD4+ T Cells Using a TGF-β-containing Protocol

In Vitro Differentiation of Human CD4⁺FOXP3⁺ Induced Regulatory T Cells (iTregs) from Naïve CD4⁺ T Cells Using a TGF-β-containing Protocol

Published on: December 30, 2016

[SOX4驱动CD4⁺T细胞向免疫抑制表型的分化]

Yuelu Zhang¹, Ziqi Tao¹, Xi Huang¹

¹Department of Laboratory Medicine, the First Affiliated Hospital of Nanjing Medical University, Branch of National Clinical Research Center for Laboratory Medicine, the First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.

Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology

|February 1, 2026

概括

SRY盒转录因子4 (SOX4) 在CD4+T细胞中促进了类似T细胞的调节状态. SOX4增强了它们的氧化酸化 (OXPHOS) 并调节了免疫抑制分子.

科学领域:

免疫学免疫学免疫学
细胞生物学细胞生物学
代谢过程中的代谢.

背景情况:

CD4+ T 细胞在免疫调节中起着至关重要的作用.
氧化酸化 (OXPHOS) 对T细胞功能和新陈代谢至关重要.
在CD4+T细胞分化和新陈代谢中SRY盒转录因子4 (SOX4) 的作用仍未得到充分研究.

研究的目的:

研究SOX4对CD4+T细胞分化的调控作用.
确定SOX4对CD4+T细胞中OXPHOS代谢的影响.

主要方法:

对于SOX4过度表达 (SOX4-OE) 的人类外围CD4+T细胞的隔离和lentiviral转导.
对表型标记物,转录因子,细胞因子和OXPHOS指标的流细胞计分析.
RNA测序 (RNA-seq) 用于差异基因表达分析和途径丰富 (KEGG,GO,GSEA).

主要成果:

过度表达SOX4增加了表达激活标记 (CD25,GITR) 和抑制分子 (CTLA-4,PD-1) 的CD4+T细胞.
SOX4-OE上调调节了FOXP3,TGF-β1,IFN-γ和IL-17A,同时降低了IL-10.
RNA-seq显示了OXPHOS通路的显著丰富,增强了ATP生产,增加了线粒体呼吸链复合体,并降低了ROS/mtROS水平.

结论:

在CD4+T细胞中,SOX4会诱导一种类似于塑性调节性T细胞 (Treg) 的状态.
SOX4调节了参与Treg抑制功能的关键分子.
SOX4 增强了 CD4+ T 细胞的氧化酸化能力.

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