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艾滋病毒EP1通过重编程T_H17细胞中的聚胺代谢来加剧NASH

Yidan Ren¹, Xiaoyan Liu¹, Maoxiao Feng¹

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

Science translational medicine

|October 22, 2025

概括

研究人员确定了T助手17 (T_H17) 细胞是非酒精性脂肪肝炎 (NASH) 进展的关键驱动因素. 在T_H17细胞中准HIVEP1和ODC1可能为NASH提供新的治疗策略.

科学领域:

免疫学免疫学免疫学
肝病学肝病学是一种肝病学.
分子生物学分子生物学

背景情况:

非酒精性脂肪肝炎 (NASH) 是一种炎症性肝病,可导致肝硬化和肝癌.
驱动非酒精性脂肪性肝病 (NAFLD) 到NASH的进展的特定免疫细胞和机制尚未完全理解.

研究的目的:

研究免疫细胞在从NAFLD过渡到NASH中的作用.
为了确定关键的分子参与者和涉及到NASH病变的途径.

主要方法:

转移酶可访问的染色体测序 (scATAC-seq) 的单细胞测定,以分析NASH肝脏中的免疫细胞群.
分析scATAC-seq和单细胞RNA测序 (scRNA-seq) 数据,以确定调节性转录因子.
在小鼠模型中关键基因的遗传淘汰和代谢酶的药理抑制.

主要成果:

确定T辅助细胞17 (T_H17) 细胞是NASH肝脏中最丰富的免疫细胞类型.
人类免疫缺陷病毒I型增强剂结合蛋白1 (HIVEP1) 被发现是调节T_H17细胞功能的关键转录因子.
在小鼠中,HIVEP1的淘汰损害了T_H17细胞分化,并缓解了NASH的发展.
艾滋病毒EP1调节素脱碳酶1 (ODC1),这是聚胺代谢中的关键酶,影响T _{H _{17细胞活性.}}
抑制ODC1降低了炎症,并防止了NAFLD到NASH的过渡.

结论:

T_H17细胞通过HIVEP1介导的聚胺代谢调节,在NASH发展中发挥着至关重要的作用.
已确定HIVEP1和ODC1是治疗纳氏血淋病的潜在治疗点.

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