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在实验性自身免疫脑炎期间,BHLHE40调解了致病性TH17细胞和髓状细胞之间的交叉对话

Melissa E Cook¹, Irina Shchukina¹, Chih-Chung Lin¹

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

|November 7, 2023

概括

基本的螺旋环螺旋家族成员e40 (BHLHE40) 在多发性硬化症模型中驱动T助手17 (TH17) 细胞的致病性. 它的缺失减少了疾病的严重程度,并改变了中枢神经系统中免疫细胞的相互作用.

科学领域:

免疫学免疫学免疫学
神经科学是一个神经科学.
细胞生物学细胞生物学

背景情况:

辅助T细胞17 (TH17) 细胞是多发性硬化症 (MS) 和实验性自身免疫脑膜炎 (EAE) 病变发生的关键驱动因素.
基本螺旋环螺旋家族成员e40 (BHLHE40) 之前被确定为EAE中致病性TH细胞的标记物,其T细胞表达对疾病进展至关重要.

研究的目的:

调查BHLHE40在TH17细胞功能中的作用和EAE期间脑性.
探索BHLHE40在EAE期间对中枢神经系统 (CNS) 中髓状细胞反应的影响.

主要方法:

利用双记者小鼠在EAE期间跟踪T细胞中的BHLHE40表达.
采用Il17a-Cre介导的删除方法,专门从TH17细胞中去除BHLHE40.
在EAE期间进行了透到中枢神经系统的白细胞的单细胞RNA测序.

主要成果:

在EAE诱导后的TH1/17和前TH17细胞中证实了BHLHE40表达.
在TH细胞中删除BHLHE40导致EAE严重程度减弱,TH细胞细胞因子生产减少.
单细胞RNA测序揭示了中枢神经系统中不同的髓状细胞种群,这取决于TH17细胞中BHLHE40的存在或不存在.

结论:

BHLHE40在促进TH17细胞介导脑性方面发挥着至关重要的作用.
在活跃的EAE期间,BHLHE40影响和指导髓状细胞反应,有助于疾病的发病.

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