Chinese Team Publishes Revolutionary New Cancer Strategy in Nature: Developing a Novel Cancer Vaccine
Release time:
2026-01-19
Amid continuous breakthroughs in cancer immunotherapy, how to dismantle tumors’ ability to “hide” from the immune system has become a key focus for researchers worldwide. On January 7, a joint team from Shenzhen Bay Laboratory and Peking University published a groundbreaking study in Nature, introducing a novel strategy called “intratumoral vaccine chimera” (iVAC). This approach, for the first time, simultaneously achieves immune checkpoint blockade and efficient antigen presentation within tumors, effectively “reprogramming” cancer cells to become allies of the immune system and opening new avenues for treating immunologically “cold” tumors.
Tumors can evade immune attacks through mechanisms such as high expression of immunosuppressive molecules like PD-L1, reducing tumor antigens, and interfering with antigen presentation. While existing immune checkpoint blockade (ICB) therapies are transformative, their efficacy remains limited due to the insufficient number of functional tumor-specific T cells. Meanwhile, vaccines and adoptive T-cell therapies often fail due to the strong immunosuppressive tumor microenvironment, necessitating new strategies for in situ immune activation.
The study was jointly supervised by Professor Chen Peng of Shenzhen Bay Laboratory/Peking University, Associate Researcher Zhang Heng of Shenzhen Bay Laboratory, and Professor Xi Jianzhong of Peking University. Postdoctoral researcher Han Yu and doctoral students Ma Yicong and Pei Miao served as co-first authors. Building on their previously developed membrane protein-targeted degradation platform (meTPD), the team innovatively constructed a bifunctional molecule, iVAC, capable of simultaneously degrading PD-L1 and promoting antigen presentation.
iVAC consists of covalently linked PD-L1-degrading units and immunogenic antigens. When injected into tumors, it not only releases the immune “brake” but also induces tumor cells to exhibit antigen-presenting cell (APC)-like properties, thereby activating tumor-specific CD8+ T cells, triggering a robust immune response, reshaping the immunosuppressive microenvironment, and establishing long-term immune memory.
Due to severe deficiencies in antigen presentation within tumor regions, T cells struggle to recognize cancer cells, leading to immune silence. The innovation of iVAC lies in its “local sourcing” approach—reprogramming tumor cells in situ to endow them with antigen-presenting capabilities, transforming them from immune escapees into immune activators and fundamentally reversing tumor immune tolerance. Studies show that T cells activated by iVAC effectively eliminate tumors, shift the tumor microenvironment (TME) from an immunosuppressive to a pro-inflammatory state, release more immune effectors, and activate broader anti-tumor responses.
Using cytomegalovirus (CMV) antigens as the basis for iVAC, the team systematically validated its efficacy in in vitro cell cultures, humanized mouse models, and patient-derived tumor models. Significant tumor regression and T-cell activation were observed in all cases, with no significant systemic immune side effects, demonstrating its good controllability.
This study integrates chemical biology, immune engineering, and tumor microenvironment regulation, achieving for the first time the combined functions of “degradation + presentation” in a single strategy. It is hailed as a pioneering work in “degradation-based vaccines,” expanding the design concepts for personalized tumor vaccines and providing a feasible solution for treating immunologically cold tumors, a long-standing challenge in clinical practice.
Published in Nature, this research marks a shift in tumor immunotherapy from “target blockade” to “cellular fate reprogramming.” With ongoing optimization and clinical exploration of the iVAC platform, it holds promise as a core tool for the next generation of immunotherapies, offering new hope to millions of cancer patients.
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