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Fever supports CD8+ effector T cell responses by promoting mitochondrial translation

MPG-Autoren

O'Sullivan,  David
Department Immunometabolism, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Stanczak,  Michal A
Department Immunometabolism, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Villa,  Matteo
Department Immunometabolism, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Corrado,  Mauro
Department Immunometabolism, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Geltink,  Ramon I Klein
Department Immunometabolism, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Sanin,  David E
Department Immunometabolism, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Apostolova,  Petya
Department Immunometabolism, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Rana,  Nisha
Department Immunometabolism, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Edwards-Hicks,  Joy
Department Immunometabolism, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Grzes,  Katarzyna M
Department Immunometabolism, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Kabat,  Agnieszka M
Department Immunometabolism, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Kyle,  Ryan L
Department Immunometabolism, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Curtis,  Jonathan D
Department Immunometabolism, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Buck,  Michael D
Department Immunometabolism, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Patterson,  Annette E
Department Immunometabolism, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Field,  Cameron S
Department Immunometabolism, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Baixauli,  Francesc
Department Immunometabolism, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Puleston,  Daniel J
Department Immunometabolism, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Pearce,  Edward Jonathen
Department Immunometabolism, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

/persons/resource/persons201431

Pearce,  Erika Laine
Department Immunometabolism, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Externe Ressourcen

https://www.pnas.org/doi/full/10.1073/pnas.2023752118
(Verlagsversion)

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10.1073_pnas.2023752118.pdf
(Verlagsversion), 2MB

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Zitation

O'Sullivan, D., Stanczak, M. A., Villa, M., Uhl, F. M., Corrado, M., Geltink, R. I. K., et al. (2021). Fever supports CD8+ effector T cell responses by promoting mitochondrial translation. Proceedings of the National Academy of Sciences of the United States of America, 118: e2023752118. doi:10.1073/pnas.2023752118.


Zitierlink: https://hdl.handle.net/21.11116/0000-000D-1ACD-0
Zusammenfassung
Fever can provide a survival advantage during infection. Metabolic processes are sensitive to environmental conditions, but the effect of fever on T cell metabolism is not well characterized. We show that in activated CD8+ T cells, exposure to febrile temperature (39°C) augmented metabolic activity and T cell effector functions, despite having a limited effect on proliferation or activation marker expression. Transcriptional profiling revealed an up-regulation of mitochondrial pathways, which was consistent with increased mass and metabolism observed in T cells exposed to 39°C. Through in vitro and in vivo models, we determined that mitochondrial translation is integral to the enhanced metabolic activity and function of CD8+ T cells exposed to febrile temperature. Transiently exposing donor lymphocytes to 39°C prior to infusion in a myeloid leukemia mouse model conferred enhanced therapeutic efficacy, raising the possibility that exposure of T cells to febrile temperatures could have clinical potential.