| |||||||
ShanghaiTech University Knowledge Management System
Stress-Induced Metabolic Disorder in Peripheral CD4(+) T Cells Leads to Anxiety-like Behavior | |
Fan, Ke-qi1,2; Li, Yi-yuan1,2; Wang, Hao-li1,2; Mao, Xin-tao1,2; Guo, Jin-xin1,2; Wang, Fei1,2; Huang, Ling-jie3; Li, Yi-ning1,2; Ma, Xiang-yu4,5,6; Gao, Zheng-jun1,2; Chen, Wei7,8; Qian, Dan-dan4; Xue, Wen-jin4; Cao, Qian3; Zhang, Lei3; Shen, Li1,2; Zhang, Long1,2; Tong, Chao1,2; Zhong, Jiang-yan1,2; Lu, Wei4; Lu, Ling9; Ren, Ke-ming3; Zhong, Guisheng10 ![]() | |
2019-10-31 | |
发表期刊 | CELL (IF:45.5[JCR-2023],49.0[5-Year]) |
ISSN | 0092-8674 |
EISSN | 1097-4172 |
卷号 | 179期号:4页码:864-+ |
发表状态 | 已发表 |
DOI | 10.1016/j.cell.2019.10.001 |
摘要 | Physical or mental stress leads to neuroplasticity in the brain and increases the risk of depression and anxiety. Stress exposure causes the dysfunction of peripheral T lymphocytes. However, the pathological role and underlying regulatory mechanism of peripheral T lymphocytes in mood disorders have not been well established. Here, we show that the lack of CD4(+) T cells protects mice from stress-induced anxiety-like behavior. Physical stress-induced leukotriene B4 triggers severe mitochondrial fission in CD4(+) T cells, which further leads to a variety of behavioral abnormalities including anxiety, depression, and social disorders. Metabolomic profiles and single-cell transcriptome reveal that CD4(+) T cell-derived xanthine acts on oligodendrocytes in the left amygdala via adenosine receptor A1. Mitochondrial fission promotes the de novo synthesis of purine via interferon regulatory factor 1 accumulation in CD4(+) T cells. Our study implicates a critical link between a purine metabolic disorder in CD4(+) T cells and stress-driven anxiety-like behavior. |
收录类别 | SCI ; SCIE |
语种 | 英语 |
资助项目 | National Natural Science Foundation of China[81572651] ; National Natural Science Foundation of China[81771675] ; National Natural Science Foundation of China[81622013] ; National Natural Science Foundation of China[81700913] |
WOS研究方向 | Biochemistry & Molecular Biology ; Cell Biology |
WOS类目 | Biochemistry & Molecular Biology ; Cell Biology |
WOS记录号 | WOS:000493898000007 |
出版者 | CELL PRESS |
WOS关键词 | MITOCHONDRIAL DYNAMICS ; MICE ; AMYGDALA ; ACTIVATION ; DEPRESSION ; BRAIN ; FEAR ; DEFICIENCY ; MECHANISMS ; INHIBITORS |
原始文献类型 | Article |
引用统计 | 正在获取...
|
文献类型 | 期刊论文 |
条目标识符 | https://kms.shanghaitech.edu.cn/handle/2MSLDSTB/102232 |
专题 | iHuman研究所_PI研究组_钟桂生组 |
通讯作者 | Chai, Ren-jie; Jin, Jin |
作者单位 | 1.Zhejiang Univ, MOE Lab Biosyst Homeostasis & Protect, Hangzhou 310058, Zhejiang, Peoples R China 2.Zhejiang Univ, Life Sci Inst, Hangzhou 310058, Zhejiang, Peoples R China 3.Zhejiang Univ, Coll Med, Sir Run Run Shaw Hosp, Hangzhou 310016, Zhejiang, Peoples R China 4.Southeast Univ, Jiangsu Prov High Tech Key Lab Biomed Res, Inst Life Sci, Key Lab Dev Genes & Human Dis,Minist Educ, Nanjing 210096, Jiangsu, Peoples R China 5.Nantong Univ, Coinnovat Ctr Neuroregenerat, Nantong 226001, Peoples R China 6.Chinese Acad Sci, Inst Stem Cell & Regenerat, Beijing, Peoples R China 7.East China Normal Univ, Inst Biomed Sci, Shanghai Key Lab Regulatory Biol, 500 Dongchuan Rd, Shanghai 200241, Peoples R China 8.East China Normal Univ, Sch Life Sci, 500 Dongchuan Rd, Shanghai 200241, Peoples R China 9.Nanjing Univ, Med Sch, Nanjing Drum Tower Hosp, Dept Otolaryngol Head & Neck Surg, Nanjing 210008, Jiangsu, Peoples R China 10.ShanghaiTech Univ, iHuman Inst, Shanghai 201210, Peoples R China |
推荐引用方式 GB/T 7714 | Fan, Ke-qi,Li, Yi-yuan,Wang, Hao-li,et al. Stress-Induced Metabolic Disorder in Peripheral CD4(+) T Cells Leads to Anxiety-like Behavior[J]. CELL,2019,179(4):864-+. |
APA | Fan, Ke-qi.,Li, Yi-yuan.,Wang, Hao-li.,Mao, Xin-tao.,Guo, Jin-xin.,...&Jin, Jin.(2019).Stress-Induced Metabolic Disorder in Peripheral CD4(+) T Cells Leads to Anxiety-like Behavior.CELL,179(4),864-+. |
MLA | Fan, Ke-qi,et al."Stress-Induced Metabolic Disorder in Peripheral CD4(+) T Cells Leads to Anxiety-like Behavior".CELL 179.4(2019):864-+. |
条目包含的文件 | ||||||
文件名称/大小 | 文献类型 | 版本类型 | 开放类型 | 使用许可 |
修改评论
除非特别说明,本系统中所有内容都受版权保护,并保留所有权利。