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TRIM11通过AIM2的p62-选择性自降解来减弱Treg细胞的分化

Ting Yu¹, Xiaofang Yang², Qiang Fu³

¹The Second Affiliated Hospital, The State Key Laboratory of Respiratory Disease, Guangdong Provincial Key Laboratory of Allergy & Clinical Immunology, Guangzhou Medical University, Guangzhou, China; Department of Pharmacy, Hainan General Hospital/Hainan Affiliated Hospital of Hainan Medical University, Haikou, Hainan, China.

|October 7, 2023

概括

三方基因含有基因11 (TRIM11) 负调节调节性T (Treg) 细胞分化,并通过降解在黑色素瘤2 (AIM2) 中缺席的自身免疫性疾病. 准TRIM11可能为自身免疫性疾病提供新的治疗方法.

科学领域:

免疫学免疫学免疫学
分子生物学分子生物学
细胞生物学细胞生物学

背景情况:

乌比基化是一种关键的蛋白质修饰,调节CD4+T细胞的分化和功能.
大多数E3泛素酶在CD4+T细胞分化和相关病理中的作用尚未完全理解.

研究的目的:

为了研究三方基因含有基因11 (TRIM11) 在CD4+T细胞分化和自身免疫性疾病中的功能.
阐明TRIM11影响调节性T (Treg) 细胞稳定的机制.

主要方法:

研究了TRIM11在CD4+T细胞分化和实验性自身免疫脑膜炎 (EAE) 模型中的作用.
利用共免疫沉和西部抹杀来研究TRIM11-AIM2相互作用和AIM2降解.
评估了AIM2对Treg细胞中信号通路 (AKT,FOXO1,MYC) 和糖解的影响.

主要成果:

TRIM11被确定为CD4+T细胞中Treg细胞分化的负调节者.
TRIM11通过在黑色素瘤2 (AIM2) 中缺席的依赖性途径促进自身免疫性疾病的发展.
TRIM11通过p62诱导AIM2的无处不在和自降解,破坏Treg细胞的稳定.
通常,AIM2会减弱AKT/FOXO1酸化,MYC信号和糖解,从而促进Treg的稳定性.

结论:

TRIM11通过向AIM2进行降解来负面调节Treg细胞分化和稳定性.
在促进自身免疫性疾病的发病过程中,TRIM11起着至关重要的作用.
TRIM11代表了治疗自身免疫性疾病和由免疫失调驱动的癌症的潜在治疗标.

关键词:

CP: 免疫学免疫学在Treg细胞分化过程中,Treg细胞分化蛋白质的翻译后修饰是蛋白质的翻译后修饰.选择性的自性降解.

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