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通过调节GM-CSF表达,GATA3诱导了Th17细胞的致病性

Matthew J Butcher¹, Rama Krishna Gurram¹, Xiaoliang Zhu¹

¹Molecular and Cellular Immunoregulation Section, Laboratory of Immune System Biology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, United States.

Frontiers in immunology

|July 14, 2023

概括

在实验性自身免疫脑膜炎 (EAE) 中,GATA3对于致病性T-bet表达Th17细胞至关重要. 早期的GATA3删除会损害脑原反应,而晚期的删除会减少GM-CSF的产生,突出显示了GATA3.

科学领域:

免疫学免疫学免疫学
神经免疫学神经免疫学
细胞和分子免疫学细胞和分子免疫学

背景情况:

通过GM-CSF的产生,T-bet表达的Th17细胞有助于实验性自身免疫脑膜炎 (EAE) 病理学.
在Th17细胞中调节GM-CSF (Csf2) 表达的机制尚不清楚.

研究的目的:

调查GATA3在EAE中T-bet表达Th17细胞的分化和致病性中的作用.
阐明控制病原性Th17细胞中Csf2表达的上游调控机制.

主要方法:

使用条件淘汰赛小鼠模型 (Cre-ERT2,hCd2-Cre,Tbx21-Cre) 在不同阶段删除 Gata3.
雇佣的收养转移EAE模型和透中枢神经系统的T细胞的RNA测序 (RNA-Seq).
分析了T-bet和RORγt表达,GM-CSF的产生,以及EAE的诱导.

主要成果:

在Th17细胞中早期的Gata3删除降低了EAE病原性和T-bet+Th17细胞的产生.
晚期Gata3删除本质上损害了EAE诱导,并减少了GM-CSF的产生,而不影响T-bet+ Th17细胞数量.
RNA-Seq确定了GATA3作为病原性Th17细胞中Egr2,Bhlhe40和Csf2表达的调节者.

结论:

在EAE中,GATA3在促进和维持T-bet表达Th17细胞的致病性方面发挥着关键的细胞内在作用.
早期的GATA3依赖基因调节对于产生新发脑性Th17反应至关重要.
在致病的Th17细胞中,GATA3调节了GM-CSF的产生,可能是通过Egr2和Bhlhe40.

关键词:

布莱赫40岁的时间在 GATA3 和 GATA3 之间.转基因-CSFF是什么意思 Th17 这是一个很好的方法.实验性的自身免疫性脑膜炎.病原性是一种病原性.

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