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Peer-reviewedCC BY-NC 4.0Oncoimmunology

Irradiated dendritic cell subsets retain key immune capabilities and anti-tumor immunity is not strictly dependent on cDC1

  • Teresa Irianto1,2,3
  • Ann-Sophie Flohr1,2,3
  • Clara Reichardt1,2,3
  • Ateeqa Ghuias1,4
  • Lisa Weissmann1,2,3
  • Detlef Freitag5
  • Lukas Amon6,7,8
  • Christian H. K. Lehmann6,9,10,11,12
  • Diana Dudziak6,12,13,14,15
  • Kai Hildner12,16
  • Stefanie Corradini2,3,12
  • Benjamin Frey1,2,3,11,12
2 more authors
  • Udo S. Gaipl1,2,3,11,12
  • Michael Rückert1,2,3
16 affiliations
  1. 1Translational Radiobiology, Department of Radiation Oncology, Uniklinikum Erlangen, Friedrich-Alexander-Universität Erlangen-Nürnberg, Erlangen, Germany
  2. 2Comprehensive Cancer Center Erlangen-EMN, Erlangen, Germany
  3. 3Department of Radiation Oncology, Uniklinikum Erlangen, Friedrich-Alexander-Universität Erlangen-Nürnberg, Erlangen, Germany
  4. 4Department of Internal Medicine 3, Rheumatology and Immunology, and Friedrich-Alexander-Universität ErlangenUniversity Hospital Erlangen, Erlangen, Germany
  5. 5Central High-Pressure Laboratory, Faculty of Engineering, Friedrich-Alexander-Universität Erlangen-Nürnberg, Erlangen, Germany
  6. 6Laboratory of Dendritic Cell Biology, Department of Dermatology, University Hospital Erlangen, Friedrich-Alexander-University of Erlangen-Nürnberg, Erlangen, Germany
  7. 7Laboratory of Immunoregulation and Mucosal Immunology, VIB Center for Inflammation Research, Ghent, Belgium
  8. 8Department of Internal Medicine and Pediatrics, Ghent University, Ghent, Belgium
  9. 9CELLIKON, Department of Dermatology, Friedrich-Alexander-University of Erlangen-Nürnberg, University Hospital Erlangen, Erlangen, Germany
  10. 10Department of Pediatrics and Adolescent Medicine, Friedrich-Alexander-University Erlangen-Nürnberg, Erlangen, Germany
  11. 11FAU Profile Center Immunomedicine (FAU I-MED), Erlangen, Germany
  12. 12Deutsches Zentrum Immuntherapie (DZI), Erlangen, Germany
  13. 13Institute of Immunology, Jena University Hospital, Jena, Germany
  14. 14Comprehensive Cancer Center Central Germany (CCCG), Jena, Germany
  15. 15Cluster of Excellence Balance of the Microverse, Friedrich Schiller University Jena, Jena, Germany
  16. 16Department of Medicine 1, Universitätsklinikum Erlangen and Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU), Erlangen, Germany
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Abstract

Radiotherapy can enhance anti-tumor immunity by modulating the tumor microenvironment. However, its direct effects on dendritic cells (DCs) as key antigen-presenting cells remain poorly studied. Although DCs are considered relatively radioresistant, their functional capacity following irradiation is controversial and likely subset-dependent. In this study, we systematically analyzed the radiosensitivity and post-irradiation functional capacity of murine bone marrow-derived conventional type 1 DCs (cDC1s), which play a pivotal role in initiating CD8+ T cell-mediated anti-tumor immunity, conventional type 2 DCs (cDC2s), and monocyte-derived DCs (MoDCs) in vitro. After irradiation, DC viability and surface marker expression were assessed. To evaluate functional competence, DCs were stimulated with high hydrostatic pressure-inactivated tumor cells in combination with the adjuvants poly I:C and α-CD40 as a model system for therapeutic tumor vaccination, and the phagocytic activity, activation, and cytokine/chemokine secretion of the DCs were analyzed. DC radiosensitivity depended strongly on both the subset and maturation state, with mature DCs showing higher radioresistance than their immature counterparts, and with immature cDC1s being particularly more susceptible. Nevertheless, surviving DCs retained their ability to phagocytose tumor cells and, upon stimulation, upregulate activation- and migration-associated markers and secrete cytokines and chemokines. In vivo, radio-immunotherapy promoted DC migration to the tumor-draining lymph node and induced DC activation, as indicated by elevated concentrations of DC-related cytokines in the peripheral blood. Within a fixed radiotherapy plus checkpoint inhibition regimen, tumor growth delay was largely preserved in Batf3−/− mice, lacking the cDC1 subset. Collectively, irradiation does not abrogate DC function, and anti-tumor immunity in radio-immunotherapy does not strictly require cDC1s.

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Cite

BibTeXRIS
BibTeX
@article{irianto2026irradiated,
  title = {{Irradiated dendritic cell subsets retain key immune capabilities and anti-tumor immunity is not strictly dependent on cDC1}},
  author = {Teresa Irianto and Ann-Sophie Flohr and Clara Reichardt and Ateeqa Ghuias and Lisa Weissmann and Detlef Freitag and Lukas Amon and Christian H. K. Lehmann and Diana Dudziak and Kai Hildner and Stefanie Corradini and Benjamin Frey and Udo S. Gaipl and Michael Rückert},
  journal = {Oncoimmunology},
  year = {2026},
  month = oct,
  doi = {10.1080/2162402x.2026.2743436},
  url = {https://doi.org/10.1080/2162402x.2026.2743436},
  note = {CC BY-NC 4.0},
}
RIS
TY  - JOUR
TI  - Irradiated dendritic cell subsets retain key immune capabilities and anti-tumor immunity is not strictly dependent on cDC1
AU  - Teresa Irianto
AU  - Ann-Sophie Flohr
AU  - Clara Reichardt
AU  - Ateeqa Ghuias
AU  - Lisa Weissmann
AU  - Detlef Freitag
AU  - Lukas Amon
AU  - Christian H. K. Lehmann
AU  - Diana Dudziak
AU  - Kai Hildner
AU  - Stefanie Corradini
AU  - Benjamin Frey
AU  - Udo S. Gaipl
AU  - Michael Rückert
PY  - 2026
DA  - 2026/10/29
JO  - Oncoimmunology
DO  - 10.1080/2162402x.2026.2743436
UR  - https://doi.org/10.1080/2162402x.2026.2743436
AB  - Radiotherapy can enhance anti-tumor immunity by modulating the tumor microenvironment. However, its direct effects on dendritic cells (DCs) as key antigen-presenting cells remain poorly studied. Although DCs are considered relatively radioresistant, their functional capacity following irradiation is controversial and likely subset-dependent. In this study, we systematically analyzed the radiosensitivity and post-irradiation functional capacity of murine bone marrow-derived conventional type 1 DCs (cDC1s), which play a pivotal role in initiating CD8+ T cell-mediated anti-tumor immunity, conventional type 2 DCs (cDC2s), and monocyte-derived DCs (MoDCs) in vitro. After irradiation, DC viability and surface marker expression were assessed. To evaluate functional competence, DCs were stimulated with high hydrostatic pressure-inactivated tumor cells in combination with the adjuvants poly I:C and α-CD40 as a model system for therapeutic tumor vaccination, and the phagocytic activity, activation, and cytokine/chemokine secretion of the DCs were analyzed. DC radiosensitivity depended strongly on both the subset and maturation state, with mature DCs showing higher radioresistance than their immature counterparts, and with immature cDC1s being particularly more susceptible. Nevertheless, surviving DCs retained their ability to phagocytose tumor cells and, upon stimulation, upregulate activation- and migration-associated markers and secrete cytokines and chemokines. In vivo, radio-immunotherapy promoted DC migration to the tumor-draining lymph node and induced DC activation, as indicated by elevated concentrations of DC-related cytokines in the peripheral blood. Within a fixed radiotherapy plus checkpoint inhibition regimen, tumor growth delay was largely preserved in Batf3−/− mice, lacking the cDC1 subset. Collectively, irradiation does not abrogate DC function, and anti-tumor immunity in radio-immunotherapy does not strictly require cDC1s.
SN  - 2162-4011
SN  - 2162-402X
ER  -