Cited by 566T-cell and B-cell ImmunologyImmune cells in cancerCancer, Hypoxia, and Metabolism

Metabolic switching and fuel choice during T‐cell differentiation and memory development

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van der Windt, Gerritje J. W., Pearce, Erika L.·2012·Immunological Reviews

Abstract

Summary: Clearance or control of pathogens or tumors usually requires T‐cell‐mediated immunity. As such, understanding the mechanisms that govern the function, maintenance, and persistence of T cells will likely lead to new treatments for controlling disease. During an immune response, T‐cell development is marked by striking changes in metabolism. There is a growing appreciation that these metabolic changes underlie the capacity of T cells to perform particular functions, and this has led to a recent focus on the idea that the manipulation of cellular metabolism can be used to shape adaptive immune responses. Although interest in this area has grown in the last few years, a full understanding of the metabolic control of T‐cell functions, particularly during an immune response in vivo , is still lacking. In this review, we first provide a basic overview of metabolism in T cells, and then we focus on recent studies providing new or updated insights into the regulation of metabolic pathways and how they underpin T‐cell differentiation and memory T‐cell development.

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Crossref · 10.1111/j.1600-065x.2012.01150.x

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  • T cell activation upregulates glucose transporter 1 through T cell receptor, CD28 and PI3K-Akt-mTOR signalling, increasing aerobic glycolysis.

    “signalling pathways involving the T cell receptor (TCR), CD28 and the PI3K–Akt–mTOR axis upregulate the expression of glucose transporter 1 (GLUT1), increasing the rate of aerobic glycolysis71,72”

    From The role of mitochondria in rheumatic diseases (2022) · cites this paper as [71]

    The “Glucose and proliferating T cells” section says TCR stimulation moves Glut1 to the cell surface, while CD28 signals increase its expression and surface localization. The “Conventional view of T-cell metabolism” section links CD28–PI3K–AKT and mTOR signaling to increased glycolysis. It does not say that TCR signaling increases Glut1 expression, or specifically that mTOR increases Glut1 expression; page numbers were not supplied. (LLM, conf=0.85)

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Authors
van der Windt, G. J. W., & Pearce, E. L.
Affiliations
  • Department of Pathology & Immunology Washington University School of Medicine St. Louis MO USA
  • Washington University in St. Louis (US)
Corresponding author
Pearce, Erika L.
Venue
Immunological Reviews
Publisher
Wiley
Published
2012-08-14
Volume
249
Issue
1
Pages
27-42
ISSN
  • 0105-2896 (ISSN-L)
  • 1600-065X
OpenAlex
W1999195849
Cited by
563
References
157
Citations by year
2026: 38 · 2025: 52 · 2024: 44 · 2023: 55 · 2022: 58 · 2021: 53 · 2020: 54 · 2019: 44 · 2018: 41 · 2017: 35 · 2016: 22 · 2015: 26 · 2014: 23 · 2013: 14 · 2012: 3
FWCI
1.95
Type
journal article
Language
en
Open access
Locations
  • Immunological Reviews (publishedVersion)
  • PubMed (publishedVersion)
  • Pure Amsterdam UMC (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
  • Data Archiving and Networked Services (DANS) (submittedVersion)
  • MPG.PuRe (Max Planck Society) (submittedVersion, other-oa)
Funders
  • Emerald Foundation
  • Nederlandse Organisatie voor Wetenschappelijk Onderzoek
  • National Institutes of Health
  • National Cancer Institute (R21CA158823)
  • National Institute of Allergy and Infectious Diseases (R01AI091965)
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
  • Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
Keywords
T cell metabolism, metabolic switch, fuel selection, T cell differentiation, memory T cells, metabolic reprogramming, adaptive immune response, T cell immunity
MeSH terms
Animals, Cell Differentiation, Energy Metabolism, Humans, Immunity, Cellular, Immunologic Memory, Lymphocyte Activation, Mitochondria, T-Lymphocytes, Cell Proliferation

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