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Updated: Jun 14, 2025

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糖溶性反应PGAM出乎意料地抑制了Th17的致病性和Th17依赖的自身免疫性

Chao Wang, Allon Wagner, Johannes Fessler

bioRxiv : the preprint server for biology

|September 4, 2024

概括

糖酸酶突变酶 (PGAM) 负面调节T助手17 (Th17) 细胞的病原性,与其他糖分解酶相反. 抑制PGAM会加剧自身免疫性疾病,突出其在T细胞代谢中的调节作用.

科学领域:

免疫学免疫学免疫学
细胞的新陈代谢
分子生物学分子生物学

背景情况:

葡萄糖代谢对于T细胞的激活和分化至关重要.
辅助性T17 (Th17) 细胞在免疫和自身免疫性疾病中起着关键作用.
单个糖解反应在Th17病原性中的具体作用尚不清楚.

研究的目的:

为了研究特定的糖解反应在Th17细胞致病性中的作用.
为了确定Th17细胞致病潜力的代谢调节者.
探索糖酸酶突变酶 (PGAM) 对Th17细胞功能和自身免疫反应的影响.

主要方法:

单细胞RNA测序 (scRNA-seq) 用于分析基因表达.
从转录基因数据估计代谢流量的指南针算法.
在Th17细胞中,糖酸酶突变酶 (PGAM) 活动的扰乱.
实验性自身免疫脑膜炎 (EAE) 的收养转移模型.
在不同的葡萄糖度下培养Th17细胞.

主要成果:

罗盘分析显示,3-糖酸盐 (3PG) 到2-糖酸盐 (2PG) 的代谢分流和Th17致病性之间存在反向相关性.
扰乱PGAM增加了促炎性细胞因子表达 (IL-2,IL-17,TNF-a) 和致病基因程序.
在EAE模型中,在Th17细胞中抑制PGAM导致自身免疫反应恶化.
在PGAM依赖基因模块中,独立于葡萄糖水平,确定了最不致病的Th17细胞状态.

结论:

糖酸盐突变酶 (PGAM) 作为Th17细胞致病性的负调节剂,其作用与其他甘油酶不同.
调节PGAM活性为由Th17细胞驱动的自身免疫疾病提供了潜在的治疗策略.
葡萄糖度影响Th17细胞代谢和转录基因程序,但PGAM的调节作用是一致的.

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