利用肿瘤细胞构建全细胞癌症疫苗的策略受到广泛关注。然而，灭活肿瘤细胞的有限免疫原性以及克服实体瘤免疫抑制的挑战阻碍了基于全细胞的癌症免疫治疗的应用。受细胞表面工程中MnO2的调节作用和材料层的时空控制能力的启发，我们通过用KMnO4灭活B16F10黑色素瘤细胞来产生锰矿化肿瘤细胞，从而开发了锰（Mn）矿化肿瘤细胞B16F10@MnO2。基于KMnO4与肿瘤细胞之间的氧化还原反应，将无定形MnO2与细胞膜结构结合形成细胞基复合材料。与甲醛固定的细胞相比，MnO2 层诱导抗原呈递细胞对表达卵清蛋白 (OVA) 的肿瘤细胞产生更强的吞噬作用，从而导致体外和体内特异性抗原呈递以及随后的免疫反应。 B16F10@MnO2 的瘤内治疗抑制了 B16F10 肿瘤的生长。此外，在B16F10@MnO2处理的荷瘤小鼠中，B16F10实体瘤内CD8 T细胞的浸润和中央记忆T细胞的比例均增加，表明适应性免疫增强。该研究为改进全细胞抗肿瘤治疗提供了一种便捷有效的方法。

The strategy of using tumor cells to construct whole-cell cancer vaccines has received widespread attention. However, the limited immunogenicity of inactivated tumor cells and the challenge of overcoming immune suppression in solid tumors have hindered the application of whole-cell-based cancer immune therapy. Inspired by the regulatory effects of MnO2 and spatiotemporal control capability of material layers in cell surface engineering, we developed a manganese (Mn)-mineralized tumor cell, B16F10@MnO2, by inactivating B16F10 melanoma cells with KMnO4 to generate manganese-mineralized tumor cells. The cell-based composite was formed by combining amorphous MnO2 with the membrane structure of cells based on the redox reaction between KMnO4 and tumor cells. The MnO2 layer induced a stronger phagocytosis of ovalbumin (OVA)-expressing tumor cells by antigen presenting cells than formaldehyde-fixed cells did, resulting in specific antigen-presentation in vitro and in vivo and subsequent immune responses. Intratumoral therapy with B16F10@MnO2 inhibited B16F10 tumor growth. Moreover, the infiltration of CD8+ T cells within B16F10 solid tumors and the proportion of central memory T cells both increased in B16F10@MnO2 treated tumor-bearing mice, indicating enhanced adaptive immunity. This study provides a convenient and effective method to improve whole-cell-based anti-tumor therapy.