题名 | ATF4 Regulates CD4(+) T Cell Immune Responses through Metabolic Reprogramming |
作者 | Yang, Xi1,3; Xia, Rui1,15; Yue, Cuihua1,4; Zhai, Wensi1,4; Du, Wenwen1,16; Yang, Qianting1,5; Cao, Huiling11,12 ![]() ![]() ![]() |
通讯作者 | Lu, Binfeng |
发表日期 | 2018-05-08
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DOI | |
发表期刊 | |
ISSN | 2211-1247
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卷号 | 23期号:6页码:1754-1766 |
摘要 | T cells are strongly regulated by oxidizing environments and amino acid restriction. How T cells reprogram metabolism to adapt to these extracellular stress situations is not well understood. Here, we show that oxidizing environments and amino acid starvation induce ATF4 in CD4(+) T cells. We also demonstrate that Atf4-deficient CD4(+) T cells have defects in redox homeostasis, proliferation, differentiation, and cytokine production. We further reveal that ATF4 regulates a coordinated gene network that drives amino acid intake, mTORC1 activation, protein translation, and an anabolic program for de novo synthesis of amino acids and glutathione. ATF4 also promotes catabolic glycolysis and glutaminolysis and oxidative phosphorylation and thereby provides precursors and energy for anabolic pathways. ATF4-deficient mice mount reduced Th1 but elevated Th17 immune responses and develop more severe experimental allergic encephalomyelitis (EAE). Our study demonstrates that ATF4 is critical for CD4(+) T cell-mediated immune responses through driving metabolic adaptation. |
相关链接 | [来源记录] |
收录类别 | |
语种 | 英语
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学校署名 | 其他
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资助项目 | NIH/National Institute of Allergy and Infectious Diseases (NIAID)[1U19A168021]
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WOS研究方向 | Cell Biology
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WOS类目 | Cell Biology
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WOS记录号 | WOS:000433292800014
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出版者 | |
来源库 | Web of Science
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引用统计 |
被引频次[WOS]:67
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成果类型 | 期刊论文 |
条目标识符 | http://sustech.caswiz.com/handle/2SGJ60CL/27729 |
专题 | 生命科学学院_生物系 南方科技大学医学院 |
作者单位 | 1.Univ Pittsburgh, Sch Med, Dept Immunol, EBST E1047,200 Lothrop St, Pittsburgh, PA 15261 USA 2.Univ Pittsburgh, Inst Canc, Pittsburgh, PA USA 3.Tsinghua Univ, Sch Med, Beijing 100084, Peoples R China 4.Soochow Univ, Affiliated Hosp 3, Dept Oncol, Changzhou 213003, Jiangsu, Peoples R China 5.Guangdong Med Coll, Peoples Hosp 3, Shenzhen Key Lab Infect & Immun, Guangdong Key Lab Emerging Infect Dis, Shenzhen 518112, Guangdong, Peoples R China 6.Soochow Univ, Inst Med Biotechnol, Dept Immunol, Suzhou 215007, Peoples R China 7.UPMC, Childrens Hosp Pittsburgh, Rangos Res Ctr, Div Immunogenet,Dept Pediat, Pittsburgh, PA USA 8.Univ Pittsburgh, Dept Chem, Pittsburgh, PA 15260 USA 9.Univ Pittsburgh, Dept Bioengn, Pittsburgh, PA 15260 USA 10.Univ Pittsburgh, Sch Med, Dept Pharmacol & Chem Biol, Pittsburgh, PA 15261 USA 11.South Univ Sci & Technol China, Dept Biol, Shenzhen 518055, Peoples R China 12.South Univ Sci & Technol China, Shenzhen Key Lab Cell Microenvironm, Shenzhen 518055, Peoples R China 13.MIT, Inst Med Engn & Sci, 77 Massachusetts Ave, Cambridge, MA 02139 USA 14.Soochow Univ, Affiliated Hosp 1, Dept Gastroenterol, Suzhou 215006, Peoples R China 15.Soochow Univ, Affiliated Hosp 2, Suzhou 215004, Jiangsu, Peoples R China 16.Soochow Univ, Affiliated Hosp 1, Dept Resp Med, Suzhou 215006, Peoples R China |
推荐引用方式 GB/T 7714 |
Yang, Xi,Xia, Rui,Yue, Cuihua,et al. ATF4 Regulates CD4(+) T Cell Immune Responses through Metabolic Reprogramming[J]. Cell Reports,2018,23(6):1754-1766.
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APA |
Yang, Xi.,Xia, Rui.,Yue, Cuihua.,Zhai, Wensi.,Du, Wenwen.,...&Lu, Binfeng.(2018).ATF4 Regulates CD4(+) T Cell Immune Responses through Metabolic Reprogramming.Cell Reports,23(6),1754-1766.
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MLA |
Yang, Xi,et al."ATF4 Regulates CD4(+) T Cell Immune Responses through Metabolic Reprogramming".Cell Reports 23.6(2018):1754-1766.
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