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通过Zeb2增强剂内的三重突变消除cDC2的发展

Tian-Tian Liu¹, Sunkyung Kim¹, Pritesh Desai²

¹Department of Pathology and Immunology, Washington University in St Louis, School of Medicine, St Louis, MO, USA.

|June 22, 2022

概括

该研究显示,转录因子NFIL3和C/EBP在Zeb2增强剂中竞争,以控制树突细胞原始细胞的分离. 这种竞争对于确定2型树突细胞 (cDC2) 和它们在T辅助细胞反应中的作用至关重要.

科学领域:

免疫学
发育生物学
转录法规

背景情况:

常见的树突细胞原始体 (CDPs) 的分化路径到cDC1和cDC2系不完全理解.
虽然已知像BATF3这样的转录因子会稳定cDC1的后期承诺,但驱动CDP分歧的初始机制仍然难以捉摸.

研究的目的:

阐明控制常见树突细胞原始体 (CDP) 分离的转录机制.
确定前cDC2电池规格的初始要求.

主要方法:

对NFIL3记者小鼠进行分析,以追踪NFIL3表达动态.
通过CUT&RUN和ChIP-seq识别内源性NFIL3结合部位.
通过CRISPR-Cas9调解,对已识别的调控元素进行了体内突变分析.
在突变小鼠中评估树突细胞发育和T辅助细胞反应.

主要成果:

NFIL3 暂时与 Zeb2 增强剂结合,在那里与 C/EBPα 和 C/EBPβ 竞争.
在这些部位,NFIL3充当抑制剂,而C/EBP则充当Zeb2表达的支持者.
破坏NFIL3- C/ EBP结合位导致骨髓原体中的Zeb2表达丧失.
这导致前cDC2规范和成熟cDC2发育的完全失败,损害T助手2反应.

结论:

在Zeb2增强器中,通过NFIL3和C/EBP的竞争机制调节了CDP分离到cDC1和cDC2系.
这一调控轴对于cDC2s的发展及其在调控T助手2免疫反应中的功能至关重要.

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