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  Dynamic Cardiolipin Synthesis Is Required for CD8+ T Cell Immunity

Corrado, M., Edwards-Hicks, J., Villa, M., Flachsmann, L. J., Sanin, P. D. E., Jacobs, M., et al. (2020). Dynamic Cardiolipin Synthesis Is Required for CD8+ T Cell Immunity. Cell Metabolism, 32, 981-995. doi:10.1016/j.cmet.2020.11.003.

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Corrado et al. 2020.pdf (Verlagsversion), 4MB
 
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2020
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Corrado, Mauro1, Autor           
Edwards-Hicks, Joy1, Autor
Villa, Matteo1, Autor           
Flachsmann, Lea J1, Autor
Sanin, Pena David Estaban1, Autor           
Jacobs, Maaike1, Autor
Baixauli Celda, Francesc1, Autor           
Stanczak, Michal1, Autor
Anderson, Eve2, Autor
Azuma, Mai1, Autor
Quintana, Andrea1, Autor
Jonathan, Curtis1, Autor           
Clapes, Thomas3, Autor           
Grzes, Katarzyna1, Autor           
Kabat, Agnieska1, Autor           
Ryan, Kyle1, Autor           
Annette, Elizabeth Patterson1, Autor           
Klein-Geltink, Ramon1, Autor           
Amulic, Borko2, Autor
Steward, Colin G2, Autor
Strathdee, Douglas2, AutorTrompouki, Eirini3, Autor           O'Sullivan, David1, Autor           Pearce, Edward Jonathen1, Autor           Pearce, Erika Laine1, Autor            mehr..
Affiliations:
1Department Immunometabolism, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society, ou_persistent22              
2External Organizations, ou_persistent22              
3Department of Cellular and Molecular Immunology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society, ou_persistent22              

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Schlagwörter: cardiolipin, mitochodria, immunometabolism, PTPMT1, Tafazzin, Barth Syndrome, immune memory, CD8 T cells
 Zusammenfassung: Mitochondria constantly adapt to the metabolic needs of a cell. This mitochondrial plasticity is critical to T cells, which modulate metabolism depending on antigen-driven signals and environment. We show here that de novo synthesis of the mitochondrial membrane-specific lipid cardiolipin maintains CD8+ T cell function. T cells deficient for the cardiolipin-synthesizing enzyme PTPMT1 had reduced cardiolipin and responded poorly to antigen because basal cardiolipin levels were required for activation. However, neither de novo cardiolipin synthesis, nor its Tafazzin-dependent remodeling, was needed for T cell activation. In contrast, PTPMT1-dependent cardiolipin synthesis was vital when mitochondrial fitness was required, most notably during memory T cell differentiation or nutrient stress. We also found CD8+ T cell defects in a small cohort of patients with Barth syndrome, where TAFAZZIN is mutated, and in a Tafazzin-deficient mouse model. Thus, the dynamic regulation of a single mitochondrial lipid is crucial for CD8+ T cell immunity.

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Sprache(n): eng - English
 Datum: 2020-12-01
 Publikationsstatus: Erschienen
 Seiten: -
 Ort, Verlag, Ausgabe: -
 Inhaltsverzeichnis: -
 Art der Begutachtung: Expertenbegutachtung
 Identifikatoren: DOI: 10.1016/j.cmet.2020.11.003
 Art des Abschluß: -

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Titel: Cell Metabolism
  Andere : Cell Metabolism
Genre der Quelle: Zeitschrift
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Ort, Verlag, Ausgabe: Cambridge, MA : Cell Press
Seiten: - Band / Heft: 32 Artikelnummer: - Start- / Endseite: 981 - 995 Identifikator: ISSN: 1550-4131
CoNE: https://pure.mpg.de/cone/journals/resource/111088195284928