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Tumor-specific in situ IL-12 expression combined with αPD-L1 suppresses melanoma growth by remodeling the tumor immune microenvironment.

Created on 01 Sep 2026

Authors

Hongwei Chen, Zheng Zhang, Xinghui Lai, Zhihao Wang, Xianzhu Yang, Jinzhi Du, Xiaojiao Du

Published in

Biomaterials science. Sep 01, 2026. Epub Sep 01, 2026.

Abstract

Interleukin-12 (IL-12) potently activates antitumor immune responses and compensates for the challenge of insufficient T cell activation and infiltration faced in immune checkpoint therapy. However, its clinical application is limited by severe systemic toxicity and the upregulation of PD-L1 on tumor cells during treatment. Here, we developed iLANpTyr-IL-12, a lipid-assisted nanoparticle system loaded with tyrosinase (Tyr) promoter-driven IL-12 plasmids, designed to achieve specific and sustained IL-12 expression exclusively in melanoma cells. The secreted IL-12 promoted dendritic cell maturation, T cell activation and proliferation, and IFN-γ secretion. Notably, iLANpTyr-IL-12 treatment upregulated PD-L1 expression on tumor cells, suggesting a negative feedback loop that supports the rationale for combination with anti-PD-L1 (αPD-L1). In a subcutaneous B16-F10 melanoma model, iLANpTyr-IL-12 monotherapy significantly enhanced tumor suppression and increased intratumoral infiltration of T cells and NKT cells, along with a decreased M2/M1 macrophage ratio. When combined with αPD-L1, it produced an enhanced antitumor effect, achieved a tumor growth inhibition rate of 83% and further augmented intratumoral CD8+ T cell infiltration. Additionally, no significant systemic toxicity or organ damage was observed. Collectively, these findings demonstrate that iLANpTyr-IL-12 enables tumor-specific IL-12 expression and, when combined with αPD-L1, provides a promising cytokine-immune checkpoint combination immunotherapy with reduced off-target toxicity.

PMID:
42676227
Bibliographic data and abstract were imported from PubMed on 01 Sep 2026.

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