I型胶原蛋白可提高树突状细胞-肿瘤融合细胞的效率和抗肿瘤活性。

Collagen I enhances the efficiency and anti-tumor activity of dendritic-tumor fusion cells.

作者信息

He Jian, Zheng Rong, Zhang Zhenghua, Tan Jie, Zhou Chaofan, Zhang Guoqing, Jiang Xinglu, Sun Qianyi, Zhou Sufang, Zheng Duo, Huang Yong, Wu Lige, Lai Zongqiang, Li Jieping, Yang Nuo, Lu Xiaoling, Zhao Yongxiang

机构信息

National Center for International Research of Biological Targeting Diagnosis and Therapy /Guangxi Key Laboratory of Biological Targeting Diagnosis and Therapy Research /Collaborative Innovation Center for Targeting Tumor Diagnosis and Therapy, Guangxi Medical University, Nanning, Guangxi, China.

Shenzhen Key Laboratory of Translational Medicine of Tumor, Department of Basic Medicine, School of Medicine, Shenzhen University, Shenzhen, Guangdong, China.

出版信息

Oncoimmunology. 2017 Aug 8;6(12):e1361094. doi: 10.1080/2162402X.2017.1361094. eCollection 2017.

Abstract

Low fusion efficiency and nominal activity of fusion cells (FCs) restrict the clinical application of dendritic cell (DC)/tumor fusion cells. Collagen I (Col I) is an interstitial collagen with a closely-knit structure used to repair damaged cell membranes. This study evaluated whether Col I could improve the fusion efficiency of polyethylene glycol (PEG)-induction and enhance the immunogenicity of fusion vaccine. DC/B16 melanoma and controlled DC/H22 hepatoma cell fusions were induced by PEG with or without Col I. Col I/PEG treatment increased the levels of DC surface molecules and the secretion of lactate, pro- and anti-inflammatory cytokines in fusion cells. Col I/PEG-treated FCs enhanced T-cell proliferation and cytotoxic T lymphocyte activity. The Col I-prepared fusion vaccine obviously suppressed tumor growth and prolonged mice survival time. Thus Col I treatment could significantly improve the efficiency of PEG-induced DC/tumor fusion and enhance the anticancer activity of the fusion vaccine. This novel fusion strategy might promote the clinical application of DC/tumor fusion immunotherapy.

摘要

低融合效率和融合细胞(FCs)的名义活性限制了树突状细胞(DC)/肿瘤融合细胞的临床应用。I型胶原(Col I)是一种结构紧密的间质胶原,用于修复受损的细胞膜。本研究评估了Col I是否能提高聚乙二醇(PEG)诱导的融合效率并增强融合疫苗的免疫原性。通过添加或不添加Col I的PEG诱导DC/B16黑色素瘤细胞和对照DC/H22肝癌细胞融合。Col I/PEG处理增加了融合细胞中DC表面分子的水平以及乳酸、促炎和抗炎细胞因子的分泌。Col I/PEG处理的FCs增强了T细胞增殖和细胞毒性T淋巴细胞活性。用Col I制备的融合疫苗明显抑制了肿瘤生长并延长了小鼠存活时间。因此,Col I处理可显著提高PEG诱导的DC/肿瘤融合效率并增强融合疫苗的抗癌活性。这种新型融合策略可能会促进DC/肿瘤融合免疫疗法的临床应用。

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