在本文中，我们介绍了一种新颖的方法，其中利用涂覆人血清白蛋白的沸石咪唑酯骨架-8（HPZ），其中包含了一种光敏剂，能够在肿瘤微环境中实现有针对性的识别，从而使锌离子浓度迅速升高，同时促进所封装光敏剂（PS）的受控释放。在生理pH 7.4下，HPZ表现为约170nm的尺寸，而在pH 6.5的酸性条件下，尺寸明显减小至不到10nm。酸性诱导的HPZ分解引发了锌离子浓度的快速增加，并对结直肠癌、乳腺癌和胰腺癌展现出强大的细胞毒性效应。此外，在激光照射下，HPZ内封装的PS引发活性氧物质的产生，协同增强了锌离子引起的细胞毒性。HPZ经静脉注射到CT26肿瘤小鼠模型中，导致CD3+CD4+辅助T细胞和CD3+CD8+细胞毒性T细胞明显扩增，并伴随CD4+CD25+Foxp3+调节性T细胞比例的降低。这些变化导致肿瘤生长显著抑制，突显了HPZ在这一实验模型中的疗效。重要的是，HPZ表现出良好的安全性特点，不对重要器官产生毒性，不导致体重减轻。因此，HPZ作为单独治疗或与多种抗癌免疫疗法联合使用具有巨大的潜力，并凸显了其在抗癌免疫疗法领域的潜力。

Herein, we introduce a novel approach involving the utilization of a human serum albumin-coated zeolite imidazolate framework-8 containing a photosensitizer (HPZ) that exhibits targeted recognition of the tumor microenvironment, enabling the rapid elevation of zinc ion concentrations while facilitating the controlled release of an encapsulated photosensitizer (PS). At a physiological pH of 7.4, HPZ demonstrates a size of approximately 170 nm, significantly decreasing to less than 10 nm under pH 6.5 acidic conditions. Acid-induced decomposition of HPZ triggers a rapid increase in zinc ion concentration, eliciting potent cytotoxic effects against colorectal, breast, and pancreatic cancers. Additionally, upon laser irradiation, the encapsulated PS within HPZ initiates the generation of reactive oxygen species, synergistically augmenting the cytotoxicity induced by zinc ions. Intravenous administration of HPZ in a CT26 tumor-bearing mouse model resulted in a notable expansion of CD3+CD4+ helper T cells and CD3+CD8+ cytotoxic T cells, accompanied by a reduction in the CD4+CD25+Foxp3+ regulatory T-cell population. These changes led to significant inhibition of tumor growth, highlighting the efficacy of HPZ in this experimental model. Importantly, HPZ exhibits favorable safety characteristics, displaying no toxicity toward vital organs and inducing no weight loss. Thus, HPZ holds immense promise as a standalone treatment or in combination with diverse anticancer immunotherapies, underscoring its potential in the field of anticancer immunotherapy.