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<p>Boron Neutron Capture Therapy (BNCT) offers selective tumor cell ablation with minimal damage to normal tissues, but its efficacy is limited by therapy-induced immunosuppression and high intratumoral H<sub>2</sub>O<sub>2</sub> levels, restricting synergy with immunotherapy. Here, we report BSA-BPA-MnO<sub>2</sub>, a tumor microenvironment-responsive, manganese-enriched nanoboron agent designed to overcome these barriers. This nanoplatform combines efficient boron delivery with Mn<sup>2+</sup>-driven Fenton-like catalysis and cGAS-STING pathway activation, amplifying BNCT-induced oxidative stress and inducing immunogenic pyroptosis alongside robust type I interferon signaling. This dual mechanism transforms BNCT from a local therapy into a systemic immune activator, enhancing dendritic cell maturation and CD8<sup>+</sup> T cell responses. Additionally, MnO₂ enables MRI-guided BNCT, integrating diagnostics and therapeutics. Notably, the platform achieves potent tumor suppression and systemic immune activation even at subclinical boron levels, offering a promising strategy for next-generation immune-integrated BNCT, particularly against melanoma.</p> Graphical Abstract <p></p>

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Manganese-enriched nanoboron agent amplifies BNCT efficacy via pyroptosis-mediated immune activation and STING pathway synergy​

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年12月20日

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  • Zhicheng Zhang,
  • Xiaoyan Sun,
  • Yaxin Qin,
  • Yufan Yang,
  • Qi Dai,
  • Xiaoyan Bao,
  • Minoru Suzuki,
  • Sheng Wang,
  • Zai Yang,
  • Zhifeng Li,
  • Min Han,
  • Donghang Xu,
  • Qichun Wei

摘要

Boron Neutron Capture Therapy (BNCT) offers selective tumor cell ablation with minimal damage to normal tissues, but its efficacy is limited by therapy-induced immunosuppression and high intratumoral H2O2 levels, restricting synergy with immunotherapy. Here, we report BSA-BPA-MnO2, a tumor microenvironment-responsive, manganese-enriched nanoboron agent designed to overcome these barriers. This nanoplatform combines efficient boron delivery with Mn2+-driven Fenton-like catalysis and cGAS-STING pathway activation, amplifying BNCT-induced oxidative stress and inducing immunogenic pyroptosis alongside robust type I interferon signaling. This dual mechanism transforms BNCT from a local therapy into a systemic immune activator, enhancing dendritic cell maturation and CD8+ T cell responses. Additionally, MnO₂ enables MRI-guided BNCT, integrating diagnostics and therapeutics. Notably, the platform achieves potent tumor suppression and systemic immune activation even at subclinical boron levels, offering a promising strategy for next-generation immune-integrated BNCT, particularly against melanoma.

Graphical Abstract