Metabolic Pathways in Immune Cell Activation and Quiescence
Open accessAbstract
Studies of immune system metabolism ("immunometabolism") segregate along two paths. The first investigates the effects of immune cells on organs that regulate whole-body metabolism, such as adipose tissue and liver. The second explores the role of metabolic pathways within immune cells and how this regulates immune response outcome. Distinct metabolic pathways diverge and converge at many levels, and, therefore, cells face choices as to how to achieve their metabolic goals. There is interest in fully understanding how and why immune cells commit to particular metabolic fates and in elucidating the immunologic consequences of reaching a metabolic endpoint by one pathway versus another. This is particularly intriguing, given that metabolic commitment is influenced not only by substrate availability but also by signaling pathways elicited by metabolites. Thus, metabolic choices in cells enforce fate and function, and this area will be the subject of this review.
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The increased degradation of key enzymes SUCLA2, ALDH2, and ACO2 is consistent with a reported shift in LPS-stimulated DCs from oxidative phosphorylation and oxygen consumption to glycolysis, glucose consumption, and lactate production.
“The increased degradation of key enzymes, such as SUCLA2, ALDH2 and ACO2, is consistent with a reported shift in LPS-stimulated DCs from oxidative phosphorylation and oxygen consumption to glycolysis, glucose consumption and lactate production (39–42).”
From Dynamic profiling of the protein life cycle in response to pathogens (2015) · cites this paper as [41]
Tumour infiltrating lymphocytes (TILs) possess attributes of glucose-deprived cells resulting in T cell dysfunction.
“tumour infiltrating lymphocytes (TILs) possess attributes of glucosedeprived cells resulting in T cell dysfunction [79].”
From Senescence of T Lymphocytes: Implications for Enhancing Human Immunity (2016) · cites this paper as [79]
ROS stabilize HIF-1α by inducing non-enzymatic decarboxylation of α-KG and by oxidizing Fe2+ to Fe3+.
“ROS-can stabilize HIF-1α by inducing non-enzymatic decarboxylation of α-KG24 and by oxidizing iron (Fe2+) to Fe3+, two required PHD co-factors25.”
From Coupling Krebs cycle metabolites to signalling in immunity and cancer (2018) · cites this paper as [24]
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References 111 · Cited by 1,692
- Authors
- Pearce, E. L., & Pearce, E. J.
- Affiliations
- Washington University in St. Louis (US)
- Corresponding author
- Pearce, Erika L.
- Pearce, Edward J.
- Venue
- Immunity
- Publisher
- Elsevier BV
- Published
- 2013-04
- Volume
- 38
- Issue
- 4
- Pages
- 633-643
- ISSN
- 1074-7613 (ISSN-L)
- PMC
- PMC3654249
- OpenAlex
- W1996235861
- Cited by
- 1,692
- References
- 111
- Citations by year
- 2026: 163 · 2025: 114 · 2024: 146 · 2023: 142 · 2022: 182 · 2021: 187 · 2020: 158 · 2019: 136 · 2018: 126 · 2017: 100 · 2016: 91 · 2015: 74 · 2014: 51 · 2013: 19
- FWCI
- 6.83
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Immunity (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Cancer Institute (R21CA158823, R01CA164062)
- National Institute of Allergy and Infectious Diseases (R01AI091965)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Keywords
- immunometabolism, immune cell metabolism, immune cell activation, metabolic reprogramming, metabolite signaling, immune regulation
- MeSH terms
- Animals, B-Lymphocytes, Cell Survival, Humans, Immune System, Immunity, Lymphocyte Activation, T-Lymphocytes, Metabolic Networks and Pathways, Cellular Microenvironment
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