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非细胞毒性纳米颗粒重塑巨噬细胞,实现肿瘤治疗的固有免疫和适应性免疫反应。

Non-cytotoxic nanoparticles re-educating macrophages achieving both innate and adaptive immune responses for tumor therapy.

作者信息

Wang Shengmei, Liu Xuanjun, Yang Minghua, Ouyang Linqi, Ding Jinsong, Wang Shengfeng, Zhou Wenhu

机构信息

Department of Pharmacy, The Third Xiangya Hospital, Central South University, Changsha, Hunan, 410013, China.

The First Hospital of Hunan University of Chinese Medicine, Changsha, Hunan, 410007, China.

出版信息

Asian J Pharm Sci. 2022 Jul;17(4):557-570. doi: 10.1016/j.ajps.2022.06.001. Epub 2022 Jun 10.

Abstract

Macrophages are important antigen-presenting cells to combat tumor via both innate and adaptive immunity, while they are programmed to M2 phenotype in established tumors and instead promote cancer development and metastasis. Here, we develop a nanomedicine that can re-educate M2 polarized macrophages to restore their anti-tumor activities. The nanomedicine has a core-shell structure to co-load IPI549, a PI3Kγ inhibitor, and CpG, a Toll-like receptor 9 agonist. Specifically, the hydrophobic IPI549 is self-assembled into a pure drug nano-core, while MOF shell layer is coated for CpG encapsulation, achieving extra-high total drugs loading of 44%. Such nanosystem could facilitate intracellular delivery of the payloads but without any cytotoxicity, displaying excellent biocompatibility. After entering macrophages, the released IPI549 and CpG exert a synergistic effect to switch macrophages from M2 to M1 phenotype, which enables anti-tumor activities via directly engulfing tumor cells or excreting tumor killing cytokines. Moreover, tumor antigens released from the dying tumor cells could be effectively presented by the re-educated macrophages owing to the up-regulation of various antigen presenting mediators, resulting in infiltration and activation of cytotoxic T lymphocytes. As a result, the nanosystem triggers a robust anti-tumor immune response in combination with PD-L1 antibody to inhibit tumor growth and metastasis. This work provides a non-cytotoxic nanomedicine to modulate tumor immune microenvironment by reprograming macrophages.

摘要

巨噬细胞是重要的抗原呈递细胞,可通过固有免疫和适应性免疫对抗肿瘤,然而在已形成的肿瘤中它们会被编程为M2表型,反而促进癌症发展和转移。在此,我们开发了一种纳米药物,它可以重塑M2极化的巨噬细胞,以恢复其抗肿瘤活性。该纳米药物具有核壳结构,可共同负载PI3Kγ抑制剂IPI549和Toll样受体9激动剂CpG。具体而言,疏水性的IPI549自组装成纯药物纳米核,同时包覆MOF壳层用于封装CpG,实现了高达44%的超高总药物负载量。这种纳米系统可以促进有效载荷的细胞内递送,但没有任何细胞毒性,显示出优异的生物相容性。进入巨噬细胞后,释放的IPI549和CpG发挥协同作用,将巨噬细胞从M2型转变为M1型,这通过直接吞噬肿瘤细胞或分泌肿瘤杀伤细胞因子实现抗肿瘤活性。此外,由于各种抗原呈递介质的上调,垂死肿瘤细胞释放的肿瘤抗原可以被重塑后的巨噬细胞有效呈递,从而导致细胞毒性T淋巴细胞的浸润和激活。因此,该纳米系统与PD-L1抗体联合触发强大的抗肿瘤免疫反应,以抑制肿瘤生长和转移。这项工作提供了一种无细胞毒性的纳米药物,通过重新编程巨噬细胞来调节肿瘤免疫微环境。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34ba/9459000/3bcc8c811d05/ga1.jpg

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