fig3

Nanomaterial-based strategies overcome PD-1 related intrinsic immune resistance

Figure 3. Therapeutic concept and in vivo effects of mPTEN@NPs in a B16F10 melanoma model. This figure illustrates mPTEN@NPs as a nanoplatform designed to restore PTEN-related antitumor activity and remodel the immunosuppressive TME, thereby helping to overcome resistance to immunotherapy. The proposed strategy enhances immune activation while reducing suppressive mechanisms associated with tumor progression. Model: B16F10 melanoma. Key readouts: tumor control, lymph node dendritic cell activation, CD8+ T-cell infiltration and effector function, reduced Treg and Mo-MDSC populations, cytokine modulation, PTEN and LC3-II expression, and ATP release. (A) Experimental timeline; (B) Tumor weights of B16F10 tumor-bearing mice treated with PTEN@NPs; (C and D) Flow cytometric analysis of the percentages of Foxp3+ CD25+ CD4+ T cells (C) and Mo-MDSCs (D); (E) Immunofluorescence imaging of PTEN (green) and LC3-II (red) in PTEN-mutated B16F10 tumor tissues. Adapted with permission from American Association for the Advancement of Science[62]. mPTEN: PTEN mRNA (PTEN: phosphatase and tensin homolog); NPs: nanoparticles; TME: tumor microenvironment; Treg: regulatory T cell; Mo-MDSC: monocytic myeloid-derived suppressor cell; ATP: adenosine triphosphate.

Cancer Drug Resistance
ISSN 2578-532X (Online)

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