非正规的NFKB信号传递通过FOXP3依赖的调节性T细胞程序赋予抑制功能
Yohei Sato1, Erika Osada1, Yoshinobu Manome1
1Core Research Facilities, Research Center for Medical Sciences, The Jikei University School of Medicine, Tokyo, Japan.
Heliyon
|December 21, 2023
概括
激活B细胞 (NFKB) 信号的非正规核因子卡帕光链增强剂,特别是NFKB2,对于通过FOXP3.3维持人类调节性T细胞 (Tregs) 的功能和表型至关重要.
科学领域:
- 免疫学 免疫学 免疫学
- 细胞生物学 细胞生物学
- 分子生物学分子生物学
背景情况:
- 调节性T细胞 (Tregs) 对于免疫系统平衡至关重要.
- 在人类Tregs中激活B细胞 (NFKB) 信号的非正规核因子"κ-光链增强剂"的作用尚不清楚.
研究的目的:
- 研究人类Tregs中NFKB信号通路的功能.
- 阐明NFKB2在维持Treg表型和功能中的作用.
主要方法:
- 使用CRISPR/Cas9.9,对Treg样细胞系 (MT-2) 和人类Tregs进行基因修饰.
- 对FOXP3表达和FOXP3依赖分子的分析.
- 对Treg抑制功能的评估.
主要成果:
- 在MT-2细胞和人类Tregs中NFKB2的淘汰导致FOXP3的下调.
- 减少FOXP3-依赖分子的表达.
- NFKB2淘汰赛人类Tregs表现出抑制功能的减弱.
结论:
- 非正规的NFKB信号传输,特别是NFKB2,对于维持Treg表型和抑制功能至关重要.
- 这种维护是通过FOXP3依赖的调节性T细胞程序实现的.
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