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缺少RIPK1可以阻止胸膜NK1.1的表达和随后的iNKT细胞发育

Thomas Hägglöf^1,2, Raksha Parthasarathy¹, Nathaniel Liendo^1,3

¹Department of Microbiology, Immunology & Molecular Genetics, University of Texas Health at San Antonio, San Antonio, TX, United States.

Frontiers in immunology

|November 15, 2023

概括

受体相互作用蛋白激酶1 (RIPK1) 和酶-8 (Casp8) 对T细胞的发育和功能至关重要. 在RIPK1中使用.

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:

受体相互作用蛋白激酶1 (RIPK1) 和酶-8 (Casp8) 是细胞亡和T细胞发育的关键调节者.
RIPK1的突变与人类的自身炎症性疾病有关,包括切割抵抗性RIPK1诱导的自身炎症 (CRIA) 和炎症性肠病.
此外,RIPK1在T细胞分化和恒温中也起着细胞死亡独立的作用.

研究的目的:

研究RIPK1在T细胞发育和恒温的体内功能,特别是在RIPK3和Caspase-8缺乏的背景下.
阐明RIPK1在iNKT细胞发育中的作用,NK1.1表达和细胞因子效应反应.
确定RIPK1的激酶或支架功能是否对iNKT细胞调节至关重要.

主要方法:

利用Ripk3和Casp8缺乏的小鼠,使Ripk1缺乏的小鼠能够在体内研究中存活到成年.
进行体内和体外刺激试验,以评估iNKT细胞的发育,NK1.1表达和细胞因子的产生.
在野生型,DKO (Casp8-,Ripk3-缺乏) 和TKO (Ripk1-,Casp8-,Ripk3-缺乏) 小鼠以及表达酶死亡RIPK1 (RIPK1kd) 的小鼠中比较了iNKT细胞表型.

主要成果:

RIPK1对于体iNKT细胞的NK1.1表达至关重要,这是它们发育和从第二阶段过渡到第三阶段的关键阶段.
无论是RIPK1还是Casp8,都调解了iNKT细胞的细胞因子效应反应.
在DKO和TKO小鼠中观察到扩张和过度激活的iNKT毛囊辅助细胞 (iNKTFH),这表明RIPK1和Casp8在调节iNKTFH细胞平衡中的作用.
酶死亡的RIPK1 (RIPK1kd) 没有表现出发育或功能性iNKT细胞异常,突出显示了RIPK1的支架功能的重要性.

结论:

RIPK1独特地调节胸膜iNKT细胞的发育,可能是通过其支架功能来响应T细胞受体参与.
RIPK1和Casp8共同调节iNKT细胞的作用因子功能.
用小分子抑制剂向RIPK1可能通过调节iNKT细胞的发育和功能来为自身炎症状况提供治疗策略.

关键词:

在 NK1.1+ 细胞中.在RIPK1中使用.在RIPK3中使用RIPK3.在Caspase 8中使用.在iNKT细胞发育过程中.

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