DNA exonuclease Trex1 regulates radiotherapy-induced tumour immunogenicity
Open accessAbstract
Radiotherapy is under investigation for its ability to enhance responses to immunotherapy. However, the mechanisms by which radiation induces anti-tumour T cells remain unclear. We show that the DNA exonuclease Trex1 is induced by radiation doses above 12–18 Gy in different cancer cells, and attenuates their immunogenicity by degrading DNA that accumulates in the cytosol upon radiation. Cytosolic DNA stimulates secretion of interferon-β by cancer cells following activation of the DNA sensor cGAS and its downstream effector STING. Repeated irradiation at doses that do not induce Trex1 amplifies interferon-β production, resulting in recruitment and activation of Batf3-dependent dendritic cells. This effect is essential for priming of CD8 + T cells that mediate systemic tumour rejection (abscopal effect) in the context of immune checkpoint blockade. Thus, Trex1 is an upstream regulator of radiation-driven anti-tumour immunity. Trex1 induction may guide the selection of radiation dose and fractionation in patients treated with immunotherapy.
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Compelling clinical and experimental evidence support the importance of IFN-β production by tumor cells themselves in mediating antitumor responses to radiation therapy in combination with immune checkpoint inhibitors.
“Nevertheless, compelling clinical and experimental evidence support the importance of IFN-β production by tumor cells themselves in mediating antitumor responses to radiation therapy in combination with immune checkpoint inhibitors46–48.”
From Epigenetic state determines the in vivo efficacy of STING agonist therapy (2023) · cites this paper as [47]
The Discussion (page unavailable) says tumour-cell IFN-β production is essential for radiation-induced antitumour T-cell responses, and the experiments link this mechanism to abscopal responses with radiation plus anti-CTLA4. The paper provides experimental evidence, including work with human cancer cells, but does not establish clinical evidence that tumour-cell IFN-β mediates patient responses to the combination. (LLM, conf=0.85)
Experimental — accuracy not yet measuredThe importance of IFN-β production by cancer cells in the recruitment and activation of Batf3-dependent dendritic cells has been demonstrated in different settings.
“The importance of IFN-β production by cancer cells in the recruitment and activation of Batf3-dependent dendritic cells has been also demonstrated in different settings47,49.”
From Epigenetic state determines the in vivo efficacy of STING agonist therapy (2023) · cites this paper as [47]
IFN-β induction in tumor cells can exert direct effects both on tumor cells and APCs.
“IFN-β induction in tumor cells can exert direct effects both on tumor cells as well as APCs16,47.”
From Epigenetic state determines the in vivo efficacy of STING agonist therapy (2023) · cites this paper as [47]
Type I IFN is produced by cancer cells undergoing ICD via TLR3 detection of endogenous dsRNA or cGAS detection of dsDNA.
“Type I IFN is produced by cancer cells succumbing to ICD by a mechanism involving the detection of endogenous dsRNA by TLR3 [873], or double-stranded DNA (dsDNA) by cGAS [854, 905, 906].”
From Molecular mechanisms of cell death: recommendations of the nomenclature committee on cell death 2018. (2018) · cites this paper as [854]
Defects in dsRNA/dsDNA detection (Tlr3−/−, TREX1 overexpression) or Ifnar1 deletion abolish immunogenicity of cell death triggered by various ICD inducers.
“Accordingly, defects in dsRNA or dsDNA detection imposed by genetic interventions, including the Tlr3−/− genotype and the transgene-driven overexpression of the three prime repair exonuclease 1 (TREX1), as well as the deletion of Ifnar1 from cancer or host cells, abolish the immunogenicity of cell death triggered by various ICD inducers [854, 873].”
From Molecular mechanisms of cell death: recommendations of the nomenclature committee on cell death 2018. (2018) · cites this paper as [854]
ICD can be initiated by viral infection, some FDA-approved chemotherapeutics (e.g., anthracyclines, bortezomib), specific forms of radiation therapy, and hypericin-based photodynamic therapy.
“ICD can be initiated by a relatively restricted set of stimuli, including viral infection, some FDA-approved chemotherapeutics (e.g., anthracyclines, bortezomib), specific forms of radiation therapy, and hypericin-based photodynamic therapy [854–861].”
From Molecular mechanisms of cell death: recommendations of the nomenclature committee on cell death 2018. (2018) · cites this paper as [854]
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- Authors
- Vanpouille-Box, C., Alard, A., Aryankalayil, M. J., Sarfraz, Y., Diamond, J. M., Schneider, R. J., Inghirami, G., Coleman, C. N., Formenti, S. C., & Demaria, S.
- Affiliations
- Inserm (FR)
- National Institutes of Health (US)
- Weill Cornell Medicine (US)
- New York University (US)
- Corresponding author
- Demaria, Sandra
- ORCID
- Venue
- Nature Communications
- Published
- 2017-06-09
- Volume
- 8
- Issue
- 1
- Pages
- 15618-15618
- ISSN
- 2041-1723 (ISSN-L)
- PMC
- PMC5472757
- OpenAlex
- W2624275086
- Cited by
- 1,834
- References
- 41
- Citations by year
- 2026: 232 · 2025: 186 · 2024: 214 · 2023: 220 · 2022: 208 · 2021: 241 · 2020: 224 · 2019: 159 · 2018: 114 · 2017: 35 · 2015: 1
- FWCI
- 64.12
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Nature Communications (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- U.S. Department of Defense (W81XWH1310012, W81XWH, W81XWH-13)
- Breast Cancer Research Foundation (S10 RR027619)
- Chemotherapy Foundation
- York University
- National Institutes of Health (UL1TR000038, NIH-R01, W81XWH, TR000038, UL1TR001445)
- Weill Cornell Medical College
- National Cancer Institute (CA201246, R01CA201246, P30CA016087)
- National Center for Research Resources (S10RR027619)
- National Center for Advancing Translational Sciences
- Topics
- Health Sciences › Medicine › Oncology › Cancer Immunotherapy and Biomarkers
- Life Sciences › Immunology and Microbiology › Immunology › Immunotherapy and Immune Responses
- Life Sciences › Immunology and Microbiology › Immunology › interferon and immune responses
- Keywords
- TREX1, DNA exonuclease, radiotherapy, tumor immunogenicity, cytosolic DNA, interferon-beta, cGAS-STING pathway, CD8+ T cells, abscopal effect, immune checkpoint blockade, radiation dose and fractionation, cancer immunotherapy
- MeSH terms
- STING Protein, Cyclic Guanosine Monophosphate-Adenosine Monophosphate Synthase, Animals, Dendritic Cells, Exodeoxyribonucleases, Female, Gene Expression Regulation, Humans, Immunotherapy, Membrane Proteins, Mice, Inbred BALB C, Mice, Inbred C57BL, Neoplasms, Nucleotidyltransferases, Phosphoproteins, Repressor Proteins, Mammary Neoplasms, Animal, Mice, SCID, Mice, Inbred NOD, Interferon-beta, Mice, Knockout, CD8-Positive T-Lymphocytes, Cell Line, Tumor, Basic-Leucine Zipper Transcription Factors, Mice, Receptor, Interferon alpha-beta, HEK293 Cells, CTLA-4 Antigen
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.
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