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氨酸可以增强自身免疫性甲状腺炎中的cGAS-STING-NLRP3通路

Xin Shen^1,2, Tingting Feng³, Shangbin Li⁴

¹Department of General Practice, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong Province, 250021, China.

Journal of translational autoimmunity

|April 14, 2025

概括

分支链氨基酸 (BCAA) 可能导致自身免疫性甲状腺炎 (AIT). 氨酸 (Leu) 通过激活炎症通路来加剧AIT,这表明氨酸剥夺是潜在的治疗方法.

科学领域:

免疫学免疫学免疫学
代谢学代谢学代谢学
遗传学遗传学是一个

背景情况:

分链氨基酸 (BCAA) 对于免疫调节至关重要.
在自身免疫性甲状腺炎 (AIT) 病原发生过程中,BCAA的作用基本上是未知的.
这项研究调查了BCAA和AIT之间的因果关系.

研究的目的:

使用孟德尔随机化来确定BCAA和AIT之间的因果关系.
在体外探索BCAA在cGAS-STING-NLRP3通路中的作用.
为了研究白对AIT病原体的特定影响.

主要方法:

两个样本的门德尔随机化 (MR) 用来评估因果关系.
在体外实验中使用了脂多糖 (LPS) 诱导的甲状腺毛囊细胞 (TFC).
研究了BCAA和白素缺乏对炎症标志物和细胞通路的影响.

主要成果:

BCAA被确定为AIT的致病因子 (OR = 4.960,P = 0.007).
氨酸 (Leu) 通过增加炎症性细胞因子 (TNF-α,IL-6),细胞损伤和氧化应激,显著恶化了AIT.
莱激活了Sestrin2/mTOR和cGAS-STING-NLRP3通路,而莱剥夺则抑制了这些通路.

结论:

基因预测的白水平显示出对AIT的潜在因果作用.
氨酸通过Sestrin2/mTOR和cGAS-STING-NLRP3信号通道加剧了AIT.
氨酸剥夺为AIT提供了潜在的治疗策略.

关键词:

自免疫性甲状腺炎的发生.叶氨酸 (Leucine) 是一种蛋白质.门德尔的随机化在NLRP3中,NLRP3是NLRP3中的一个.刺痛是一种刺痛.cGAS 是一个气体.

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