Impaired mitochondrial oxidative phosphorylation limits the self-renewal of T cells exposed to persistent antigen
Open accessAbstract
The majority of tumor-infiltrating T cells exhibit a terminally exhausted phenotype, marked by a loss of self-renewal capacity. How repetitive antigenic stimulation impairs T cell self-renewal remains poorly defined. Here, we show that persistent antigenic stimulation impaired ADP-coupled oxidative phosphorylation. The resultant bioenergetic compromise blocked proliferation by limiting nucleotide triphosphate synthesis. Inhibition of mitochondrial oxidative phosphorylation in activated T cells was sufficient to suppress proliferation and upregulate genes linked to T cell exhaustion. Conversely, prevention of mitochondrial oxidative stress during chronic T cell stimulation allowed sustained T cell proliferation and induced genes associated with stem-like progenitor T cells. As a result, antioxidant treatment enhanced the anti-tumor efficacy of chronically stimulated T cells. These data reveal that loss of ATP production through oxidative phosphorylation limits T cell proliferation and effector function during chronic antigenic stimulation. Furthermore, treatments that maintain redox balance promote T cell self-renewal and enhance anti-tumor immunity. Thompson and colleagues show that repetitive antigenic stimulation within the tumor environment triggers mitochondrial dysfunction by inhibiting oxidative phosphorylation, which leads to T cell exhaustion.
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Both oxidative and ER stress have been shown to contribute to T cell dysfunction across different tumor types.
“Even though both oxidative and ER stress have been shown to contribute to T cell dysfunction across different tumor types (44-51),”
From Bile acid synthesis impedes tumor-specific T cell responses during liver cancer (2025) · cites this paper as [50]
The Results section (“Mitochondrial uncoupling suppresses T cell self-renewal”; page unavailable) links oxidative stress to impaired T cell proliferation and self-renewal and reports oxidative-stress signatures in exhausted T cells from patients with melanoma, basal cell carcinoma, and squamous cell carcinoma. The paper does not establish that ER stress contributes to T cell dysfunction, so it supports only the oxidative-stress part of the sentence. (LLM, conf=0.88)
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- Authors
- Vardhana, S. A., Hwee, M. A., Berisa, M., Wells, D. K., Yost, K. E., King, B., Smith, M., Herrera, P. S., Chang, H. Y., Satpathy, A. T., van den Brink, M. R. M., Cross, J. R., & Thompson, C. B.
- Affiliations
- Memorial Sloan Kettering Cancer Center (US)
- Parker Institute for Cancer Immunotherapy (US)
- Stanford Medicine (US)
- Howard Hughes Medical Institute (US)
- Corresponding author
- Thompson, Craig B.
- ORCID
- Venue
- Nature Immunology
- Published
- 2020-07-13
- Volume
- 21
- Issue
- 9
- Pages
- 1022-1033
- ISSN
- 1529-2908 (ISSN-L)
- 1529-2916
- PMC
- PMC7442749
- OpenAlex
- W3040911066
- Semantic Scholar
- 0e26544b84036d0da9a73a3a38337fc7b1573819
- Cited by
- 575
- References
- 67
- Citations by year
- 2026: 133 · 2025: 117 · 2024: 112 · 2023: 90 · 2022: 68 · 2021: 46 · 2020: 9
- FWCI
- 18.62
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- Nature Immunology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Howard Hughes Medical Institute
- National Institutes of Health (1r01hl147584-01a1)
- National Heart, Lung, and Blood Institute (R01‐HL147584)
- National Cancer Institute (K08CA237731, P30CA008748)
- National Institute of Allergy and Infectious Diseases (R25AI140472)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Health Sciences › Medicine › Oncology › Cancer Immunotherapy and Biomarkers
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Keywords
- T cell exhaustion, mitochondrial oxidative phosphorylation, T cell self-renewal, chronic antigenic stimulation, T cell proliferation, mitochondrial oxidative stress, antioxidant treatment, redox homeostasis, tumor-infiltrating T cells, antitumor immunity
- MeSH terms
- Cell Self Renewal, Adenosine Diphosphate, Animals, Antigens, Neoplasm, Antioxidants, Energy Metabolism, Immune Tolerance, Lymphocyte Activation, Melanoma, Experimental, Mice, Inbred C57BL, Mitochondria, Neoplasms, Oxidative Phosphorylation, Lymphocytes, Tumor-Infiltrating, Clonal Anergy, CD8-Positive T-Lymphocytes, Cell Proliferation, Mice
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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