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Journal Article

Polyamine metabolism is a central determinant of helper T cell lineage fidelity

MPS-Authors

Puleston,  Daniel J
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;

Sanin,  David E
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;

Villa,  Matteo
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;

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

Weiss,  Hauke J
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;

Piletic,  Klara
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;

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

Haessler,  Fabian
Department Immunometabolism, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Musa,  Yaarub
Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Schimmelpfennig,  Lena
Department Immunometabolism, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Flachsmann,  Lea
Department Immunometabolism, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Mittler,  Gerhard
Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

/persons/resource/persons241896

Büscher,  Jörg Martin
Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

/persons/resource/persons201435

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

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

External Resource

https://www.sciencedirect.com/science/article/pii/S009286742100708X?via%3Dihub
(Publisher version)

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Fulltext (public)

10.1016_j.cell.2021.06.007.pdf
(Publisher version), 9MB

Supplementary Material (public)
There is no public supplementary material available
Citation

Puleston, D. J., Baixauli, F., Sanin, D. E., Edwards-Hicks, J., Villa, M., Kabat, A. M., et al. (2021). Polyamine metabolism is a central determinant of helper T cell lineage fidelity. Cell, 184, 4186-4202. doi:10.1016/j.cell.2021.06.007.


Cite as: https://hdl.handle.net/21.11116/0000-000D-1803-5
Abstract
Polyamine synthesis represents one of the most profound metabolic changes during T cell activation, but the biological implications of this are scarcely known. Here, we show that polyamine metabolism is a fundamental process governing the ability of CD4+ helper T cells (TH) to polarize into different functional fates. Deficiency in ornithine decarboxylase, a crucial enzyme for polyamine synthesis, results in a severe failure of CD4+ T cells to adopt correct subset specification, underscored by ectopic expression of multiple cytokines and lineage-defining transcription factors across TH cell subsets. Polyamines control TH differentiation by providing substrates for deoxyhypusine synthase, which synthesizes the amino acid hypusine, and mice in which T cells are deficient for hypusine develop severe intestinal inflammatory disease. Polyamine-hypusine deficiency caused widespread epigenetic remodeling driven by alterations in histone acetylation and a re-wired tricarboxylic acid (TCA) cycle. Thus, polyamine metabolism is critical for maintaining the epigenome to focus TH cell subset fidelity.