平衡
生物
细胞生物学
T细胞
免疫系统
炎症
表型
葡萄糖稳态
线粒体
效应器
免疫学
遗传学
基因
胰岛素抵抗
胰岛素
内分泌学
作者
Toshio Kanno,Takahiro Nakajima,Yusuke Kawashima,Satoru Yokoyama,Hikari K. Asou,Shigemi Sasamoto,Koji Hayashizaki,Yuki Kinjo,Osamu Ohara,Toshinori Nakayama,Yusuke Endo
出处
期刊:Cell Reports
[Elsevier]
日期:2021-11-01
卷期号:37 (6): 109921-109921
被引量:15
标识
DOI:10.1016/j.celrep.2021.109921
摘要
Summary
Regulatory T (Treg) cells are critical for immunological tolerance and immune homeostasis. Treg cells strongly rely on mitochondrial metabolism and show a lower level of glycolysis. However, little is known about the role of lipid metabolism in the regulation of Treg cell homeostasis. Some members of the ACSL family of acyl-coenzyme A (CoA) synthases are expressed in T cells, but their function remains unclear. A combination of RNA-sequencing and proteome analyses shows that Acsbg1, a member of ACSL, is selectively expressed in Treg cells. We show that the genetic deletion of Acsbg1 not only causes mitochondrial dysfunction, but it also dampens other metabolic pathways. The extrinsic supplementation of Acsbg1-deficient Treg cells with oleoyl-CoA restores the phenotype of the Treg metabolic signature. Furthermore, this pathway in ST2+ effector Treg cells enhances immunosuppressive capacity in airway inflammation. Thus, Acsbg1 serves as a metabolic checkpoint governing Treg cell homeostasis and the resolution of lung inflammation.
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