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调节T细胞中的AIM2抑制自身免疫性疾病

Wei-Chun Chou^1,2, Zengli Guo^1,3, Hao Guo^1,2

¹Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.

|January 28, 2021

概括

炎酶体受体AIM2在T调节细胞中具有新的作用,独立于炎酶体功能. 通过调节免疫代谢和信号通路来稳定T调节细胞,抑制自身免疫.

科学领域:

免疫学
细胞生物学
代谢过程

背景情况:

包括NLRP3在内的炎症酶激活骨髓细胞中的卡斯帕酶-1和热,从而引发炎症和自身免疫.
结合DNA的炎酶体受体AIM2主要以其在骨髓细胞炎酶体激活中的作用而闻名.
调节T细胞对于免疫平衡和预防自身免疫是至关重要的.

研究的目的:

研究AIM2在T细胞调节功能中的作用.
确定AIM2是否在T调节细胞中具有炎酶独立的功能.
阐明AIM2影响T细胞调节稳定性和免疫反应的机制.

主要方法:

测序RNA和生物化学分析以评估AIM2对T调节细胞的信号通路和代谢的影响.
分析人类和小鼠T调节细胞中的转录因子对AIM2的表达和调节.
在炎症期间评估AIM2在T细胞调节稳定性中的作用.

主要成果:

AIM2在T调节细胞中高度表达,由TGFβ诱导,并由关键的T调节细胞转录因子调节.
在T调节细胞中促进脂质氧化酸化的同时,AIM2减弱了AKT酸化,mTOR和MYC信号和糖解.
AIM2 与RACK1- PP2A复合体相互作用以抑制AKT酸化,从而在炎症期间增强T调节细胞的稳定性.

结论:

在T细胞调节功能中,AIM2具有关键的T细胞内在和炎症体独立作用.
通过调节AKT-mTOR信号和改变免疫代谢来促进T调节细胞的稳定性,AIM2抑制了自身免疫.
这些发现揭示了AIM2在适应性免疫中的新功能,与其在先天免疫中的既定作用不同.

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