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炎症性巨细胞通过减少线粒体翻译来重新编程免疫抑制

Marlies Cortés¹, Agnese Brischetto², M C Martinez-Campanario²

¹Group of Gene Regulation in Stem Cells, Cell Plasticity, Differentiation, and Cancer, IDIBAPS, 08036, Barcelona, Spain. mcortesh@recerca.clinic.cat.

Nature communications

|November 18, 2023

概括

塑性因子ZEB1对于通过重编程巨细胞来启动和解决炎症至关重要. 甲福明可以模仿ZEB1的作用.

科学领域:

免疫学免疫学免疫学
细胞生物学细胞生物学
代谢过程中的代谢.

背景情况:

炎症可以消失或慢性化,由免疫细胞重编程驱动.
抗糖尿病药物梅特福林通过鲜为人知的机制影响炎症.

研究的目的:

为了研究ZEB1在美特福林抗炎作用中的作用.
阐明ZEB1在炎症解消期间巨细胞代谢重编程中的功能.

主要方法:

使用了缺少ZEB1的小鼠 (骨髓细胞特异性淘汰).
分析了人类患者样本.
研究了巨细胞的代谢和线粒体变化.
评估了mTORC1信号传导和蛋白质翻译.

主要成果:

甲福明的抗炎作用取决于巨细胞中ZEB1的表达.
通过促进免疫抑制,ZEB1对于启动和解决炎症至关重要.
ZEB1通过自细胞调节线粒体含量,并抑制线粒体翻译.
甲胺模仿ZEB1诱导的代谢重编程,抑制mTORC1信号传递和线粒体翻译.

结论:

ZEB1驱动髓状细胞的代谢可塑性,影响炎症和免疫抑制.
准ZEB1为调节炎症和免疫抑制条件提供了一个潜在的策略.

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