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  Mitochondrial Dynamics Controls T Cell Fate through Metabolic Programming

Buck, M. D., O’Sullivan, D., Geltink, R. I. K., Curtis, J. D., Chang, C.-H., Sanin, D. E., et al. (2016). Mitochondrial Dynamics Controls T Cell Fate through Metabolic Programming. Cell, 166, 63-76. doi:doi: 10.1016/j.cell.2016.05.035.

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Item Permalink: http://hdl.handle.net/11858/00-001M-0000-002C-A8CE-2 Version Permalink: http://hdl.handle.net/21.11116/0000-0005-C3ED-4
Genre: Journal Article

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 Creators:
Buck, Michael D.1, 2, Author
O’Sullivan, David1, Author
Geltink, Ramon I. Klein1, Author
Curtis, Jonathan D.1, Author
Chang, Chih-Hao2, Author
Sanin, David E.1, Author
Qiu, Jing1, 2, Author
Kretz, Oliver3, 4, Author
Braas, Daniel5, Author
van der Windt, Gerritje J.W.6, Author
Chen, Qiongyu2, Author
Huang, Stanley Ching-Cheng2, Author
O’Neill, Christina M.2, Author
Edelson, Brian T.2, Author
Pearce, Edward J.1, 7, Author              
Sesaki, Hiromi8, Author
Huber, Tobias B.3, 9, Author
Rambold, Angelika1, Author              
Pearce, Erika L.1, Author              
Affiliations:
1Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society, 79108 Freiburg, DE, ou_2243640              
2Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, USA, ou_persistent22              
3Renal Division, University Medical Center Freiburg, Freiburg, Germany, ou_persistent22              
4Department of Neuroanatomy, University of Freiburg, Freiburg, Germany, ou_persistent22              
5University of California Los Angeles Metabolomics Center, Los Angeles, USA, ou_persistent22              
6Academic Medical Center, Amsterdam, The Netherlands, ou_persistent22              
7Faculty of Biology, University of Freiburg, Freiburg, Germany, ou_persistent22              
8Department of Cell Biology, Johns Hopkins University School of Medicine, Baltimore, USA, ou_persistent22              
9BIOSS Centre for Biological Signaling Studies, Freiburg, Germany, ou_persistent22              

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 Abstract: Activated effector T (TE) cells augment anabolic pathways of metabolism, such as aerobic glycolysis, while memory T (TM) cells engage catabolic pathways, like fatty acid oxidation (FAO). However, signals that drive these differences remain unclear. Mitochondria are metabolic organelles that actively transform their ultrastructure. Therefore, we questioned whether mitochondrial dynamics controls T cell metabolism. We show that TE cells have punctate mitochondria, while TM cells maintain fused networks. The fusion protein Opa1 is required for TM, but not TE cells after infection, and enforcing fusion in TE cells imposes TM cell characteristics and enhances antitumor function. Our data suggest that, by altering cristae morphology, fusion in TM cells configures electron transport chain (ETC) complex associations favoring oxidative phosphorylation (OXPHOS) and FAO, while fission in TE cells leads to cristae expansion, reducing ETC efficiency and promoting aerobic glycolysis. Thus, mitochondrial remodeling is a signaling mechanism that instructs T cell metabolic programming.

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Language(s): eng - English
 Dates: 2016-06-30
 Publication Status: Published in print
 Pages: -
 Publishing info: -
 Table of Contents: -
 Rev. Type: Peer
 Identifiers: DOI: doi: 10.1016/j.cell.2016.05.035
 Degree: -

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Title: Cell
Source Genre: Journal
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Publ. Info: Cambridge, Mass. : Cell Press
Pages: - Volume / Issue: 166 Sequence Number: - Start / End Page: 63 - 76 Identifier: ISSN: 0092-8674
CoNE: https://pure.mpg.de/cone/journals/resource/954925463183