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Peer-reviewedCC BY-NC-ND 4.0Cell Reports Medicine

Dendritic cell centric nanoengineering couples antigen acquisition and STING activation for cancer immunotherapy

  • Shuting Xiang1
  • Shanshan Ma2,3
  • Tuzhi Xu1
  • Wenwen Yu3
  • Jiefu Wang3
  • Xin You4
  • Mengjia Chai1
  • Xiaohu Wang1
  • Xiaoliang Wang5
  • Junmei Zhang1
  • Junjia Liu1
  • Xiubao Ren2,3
4 more authors
  • Weijie Song3
  • Tingting Qin3
  • Suxin Li1
  • Jian Wang3,6
6 affiliations
  1. 1Department of Pharmaceutics, Jiang Su Key Laboratory of Drug Design and Optimization, State Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing 210009, China
  2. 2School of Medicine, Nankai University, Tianjin 300071, China
  3. 3Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, State Key Laboratory of Druggability Evaluation and Systematic Translational Medicine, Key Laboratory of Cancer Prevention and Therapy, Tianjin 300060, China
  4. 4Tianjin Central Hospital of Obstetrics and Gynecology/Nankai University Affiliated Maternity Hospital, Tianjin Key Laboratory of Human Development and Reproductive Regulation, Tianjin 300100, China
  5. 5State Key Laboratory of Druggability Evaluation and Systematic Translational Medicine, Tianjin Institute of Pharmaceutical Research, 306 Huiren Road, Tianjin 300301, P.R. China
  6. 6Haihe Laboratory of Cell Ecosystem, Tianjin 300100, China
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Abstract

Stimulator of interferon genes (STING) agonists have shown limited antitumor efficacy, in part because STING activation is not preferentially focused on dendritic cells (DCs), which specialize in cross-priming. We present a DC-centric strategy that synergistically licenses DCs by coordinating CD47-SIRPα checkpoint relief and STING activation via dual ultra-pH-sensitive gating. Mild tumor acidity first unmasks the αCD47 cue to prime antigen acquisition. Following DC-biased uptake, a second acidic gate releases cGAMP to engage STING in antigen-bearing DCs. Functionally, efficacy requires Batf3-dependent cDC1s and CD8+ T cells, yet is preserved after macrophage depletion. In murine models, this strategy suppresses tumor growth and metastasis with good tolerability, and it retains activity in a humanized cell-line-derived xenograft model established in NSG-SGM3 hosts, supporting activity in a partially reconstituted human immune setting. Together, this work presents a mechanism-guided combination strategy to optimize STING agonist therapy.

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Cite

BibTeXRIS
BibTeX
@article{xiang2026dendritic,
  title = {{Dendritic cell centric nanoengineering couples antigen acquisition and STING activation for cancer immunotherapy}},
  author = {Shuting Xiang and Shanshan Ma and Tuzhi Xu and Wenwen Yu and Jiefu Wang and Xin You and Mengjia Chai and Xiaohu Wang and Xiaoliang Wang and Junmei Zhang and Junjia Liu and Xiubao Ren and Weijie Song and Tingting Qin and Suxin Li and Jian Wang},
  journal = {Cell Reports Medicine},
  year = {2026},
  month = sep,
  doi = {10.1016/j.xcrm.2026.103025},
  url = {https://doi.org/10.1016/j.xcrm.2026.103025},
  note = {CC BY-NC-ND 4.0},
}
RIS
TY  - JOUR
TI  - Dendritic cell centric nanoengineering couples antigen acquisition and STING activation for cancer immunotherapy
AU  - Shuting Xiang
AU  - Shanshan Ma
AU  - Tuzhi Xu
AU  - Wenwen Yu
AU  - Jiefu Wang
AU  - Xin You
AU  - Mengjia Chai
AU  - Xiaohu Wang
AU  - Xiaoliang Wang
AU  - Junmei Zhang
AU  - Junjia Liu
AU  - Xiubao Ren
AU  - Weijie Song
AU  - Tingting Qin
AU  - Suxin Li
AU  - Jian Wang
PY  - 2026
DA  - 2026/09/07
JO  - Cell Reports Medicine
DO  - 10.1016/j.xcrm.2026.103025
UR  - https://doi.org/10.1016/j.xcrm.2026.103025
AB  - Stimulator of interferon genes (STING) agonists have shown limited antitumor efficacy, in part because STING activation is not preferentially focused on dendritic cells (DCs), which specialize in cross-priming. We present a DC-centric strategy that synergistically licenses DCs by coordinating CD47-SIRPα checkpoint relief and STING activation via dual ultra-pH-sensitive gating. Mild tumor acidity first unmasks the αCD47 cue to prime antigen acquisition. Following DC-biased uptake, a second acidic gate releases cGAMP to engage STING in antigen-bearing DCs. Functionally, efficacy requires Batf3-dependent cDC1s and CD8+ T cells, yet is preserved after macrophage depletion. In murine models, this strategy suppresses tumor growth and metastasis with good tolerability, and it retains activity in a humanized cell-line-derived xenograft model established in NSG-SGM3 hosts, supporting activity in a partially reconstituted human immune setting. Together, this work presents a mechanism-guided combination strategy to optimize STING agonist therapy.
SN  - 2666-3791
ER  -