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IF 29.4! Vacancy engineering ferroelectric nanomedicine for Cuprotosis/cell apoptosis co activation immunotherapy
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IF 29.4! Vacancy engineering ferroelectric nanomedicine for Cuprotosis/cell apoptosis co activation immunotherapy

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Due to the poor immunogenicity and insufficient immune cell infiltration of most tumors, the efficacy of immunotherapy is low, highlighting the importance of inducing immunogenic cell death and activating the immune system to achieve better treatment outcomes. Here, ferroelectric Bi 2 CuO 4 nanoparticles (referred to as BCO-V Cu) with abundant copper vacancies were reasonably designed and modified for ferroelectric enhanced cell apoptosis, copper apoptosis, and subsequently induced immunotherapy. In this structure, vacancies suppress the recombination of electron hole pairs and the band bending caused by ferroelectric polarization leads to high catalytic activity, triggering reactive oxygen species bursts and inducing cell apoptosis. The cell fragments produced by apoptosis serve as antigens to activate T cells. In addition, due to the electric charge generated by ferroelectric catalysis, this nanomedicine can act as an "intelligent switch", opening the cell membrane, promoting the internalization of nanomaterials, and closing the Cu+efflux pathway, causing copper apoptosis, thereby generating a strong immune response triggered by the decrease in adenosine triphosphate content. The ribonucleic acid transcription test revealed pathways associated with immune response activation. Therefore, this study first demonstrated a feasible strategy for enhancing the efficacy of immunotherapy by inducing cell apoptosis and copper apoptosis using a single ferroelectric semiconductor.

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