Sugar addiction: An Achilles’ heel of auto-immune diseases?

Dietmar M.W. Zaiss; Paul J. Coffer

doi:10.1016/j.cmet.2022.03.007

Sugar addiction: An Achilles’ heel of auto-immune diseases?

Dietmar M.W. Zaiss, Paul J. Coffer^*

^*Corresponding author for this work

Research output: Contribution to journal › Comment/Letter to the editor › Academic › peer-review

Abstract

In this issue of Cell Metabolism, Hochrein et al. identify a metabolic checkpoint controlling the transcriptional programming of effector CD4⁺ T cells. The authors show that GLUT3-mediated glucose import and ACLY-dependent acetyl-CoA generation control histone acetylation and, hence, the epigenetic imprinting of effector gene expression in differentiated effector CD4⁺ T cells. These findings suggest a novel therapeutic target for inflammation-associated diseases.

Original language	English
Pages (from-to)	503-505
Number of pages	3
Journal	Cell Metabolism
Volume	34
Issue number	4
DOIs	https://doi.org/10.1016/j.cmet.2022.03.007
Publication status	Published - 5 Apr 2022

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10.1016/j.cmet.2022.03.007

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title = "Sugar addiction: An Achilles{\textquoteright} heel of auto-immune diseases?",

abstract = "In this issue of Cell Metabolism, Hochrein et al. identify a metabolic checkpoint controlling the transcriptional programming of effector CD4+ T cells. The authors show that GLUT3-mediated glucose import and ACLY-dependent acetyl-CoA generation control histone acetylation and, hence, the epigenetic imprinting of effector gene expression in differentiated effector CD4+ T cells. These findings suggest a novel therapeutic target for inflammation-associated diseases.",

author = "Zaiss, \{Dietmar M.W.\} and Coffer, \{Paul J.\}",

note = "Publisher Copyright: {\textcopyright} 2022 Elsevier Inc.",

year = "2022",

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doi = "10.1016/j.cmet.2022.03.007",

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AU - Zaiss, Dietmar M.W.

AU - Coffer, Paul J.

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N2 - In this issue of Cell Metabolism, Hochrein et al. identify a metabolic checkpoint controlling the transcriptional programming of effector CD4+ T cells. The authors show that GLUT3-mediated glucose import and ACLY-dependent acetyl-CoA generation control histone acetylation and, hence, the epigenetic imprinting of effector gene expression in differentiated effector CD4+ T cells. These findings suggest a novel therapeutic target for inflammation-associated diseases.

AB - In this issue of Cell Metabolism, Hochrein et al. identify a metabolic checkpoint controlling the transcriptional programming of effector CD4+ T cells. The authors show that GLUT3-mediated glucose import and ACLY-dependent acetyl-CoA generation control histone acetylation and, hence, the epigenetic imprinting of effector gene expression in differentiated effector CD4+ T cells. These findings suggest a novel therapeutic target for inflammation-associated diseases.

UR - https://www.scopus.com/pages/publications/85127286209

U2 - 10.1016/j.cmet.2022.03.007

DO - 10.1016/j.cmet.2022.03.007

M3 - Comment/Letter to the editor

C2 - 35385700

AN - SCOPUS:85127286209

SN - 1550-4131

VL - 34

SP - 503

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JO - Cell Metabolism

JF - Cell Metabolism

IS - 4

ER -

Sugar addiction: An Achilles’ heel of auto-immune diseases?

Abstract

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