CELL INTELLIGENCE · 肿瘤细胞治疗研究
肿瘤细胞治疗研究
英文原题：Engineering macrophage membrane-camouflaged nanoplatforms with enhanced macrophage function for mediating sonodynamic therapy of ovarian cancer.
Engineering macrophage membrane-camouflaged nanoplatforms with enhanced macrophage function for mediating sonodynamic therapy of ovarian cancer.
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癌症免疫治疗在癌症治疗中已展现出显著疗效，并已成功应用于多种实体瘤的治疗。然而，由于免疫抑制性肿瘤微环境（TME），卵巢癌患者对免疫治疗的缓解率仍然有限。肿瘤相关巨噬细胞（TAMs）是TME中占主导地位的髓系细胞群体，其呈现促肿瘤的M2表型，并被肿瘤细胞发出的“别吃我”信号所蒙蔽。TAMs的这些特征导致吞噬激活不足。
在本研究中，我们构建了SIM@TR-NP介导的声动力与免疫治疗联合方案。SIM@TR-NPs由过表达唾液酸结合Ig样凝集素10（Siglec-10）的工程化巨噬细胞膜修饰，内部负载声敏剂4,4',4'',4'''-(卟啉-5,10,15,20-四基)四（苯甲酸）和免疫佐剂瑞喹莫德。SIM@TR-NPs可阻断“别吃我”信号以增强巨噬细胞吞噬作用，并触发TAMs向M1表型极化，从而改善免疫抑制性TME。
同时，在超声照射下，SIM@TR-NP介导的声动力治疗（SDT）触发肿瘤细胞免疫原性细胞死亡，与基于TAM的免疫治疗相结合，将“免疫冷肿瘤”转化为“免疫热肿瘤”。SIM@TR-NP介导的声动力免疫治疗在卵巢癌中表现出强效抗肿瘤疗效，并展现出改善免疫抑制性TME的巨大潜力。
本研究提出了一种协同基于TAM的抗肿瘤免疫治疗与SDT的新兴卵巢癌治疗方案。
Cancer immunotherapy has demonstrated remarkable efficacy in the treatment of cancer, and it has been successfully applied in the treatment of various solid tumors.
However, the response rates to immunotherapy in patients with ovarian cancer remain modest because of the immunosuppressive tumor microenvironment (TME). Tumor-associated macrophages (TAMs) represent the predominant myeloid cell population within the TME, which adopt the protumorigenic M2 phenotype and are blinded by the "don't eat me" signals from tumor cells. These characteristics of TAMs result in insufficient phagocytic activation. In this study, we constructed a SIM@TR-NP-mediated combination therapy of sonodynamic and immunotherapy. SIM@TR-NPs were modified by engineered macrophage membranes with overexpressed sialic acid-binding Ig-like lectin 10 (Siglec-10), and were internally loaded with sonosensitizer 4,4',4'',4'''-(porphine-5,10,15,20-tetrayl)tetrakis(benzoic acid) and immune adjuvant resiquimod.
SIM@TR-NPs can block "don't eat me" signals to enhance macrophage phagocytosis and trigger the polarization of TAMs toward the M1 phenotype, thereby improving the immunosuppressive TME.
Simultaneously, upon ultrasound irradiation, SIM@TR-NP-mediated sonodynamic therapy (SDT) triggered immunogenic cell death in tumor cells, in combination with TAM-based immunotherapy, transforming the "immune cold tumor" into an "immune hot tumor". SIM@TR-NP-mediated sonodynamic immunotherapy exhibited potent antitumor efficacy in ovarian cancer and exhibited substantial potential for improving the immunosuppressive TME.
This study presents an emerging therapeutic regimen for ovarian cancer that synergizes TAM-based antitumor immunotherapy and SDT.
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