Department of Molecular Biology and Key Laboratory of Experimental Animal, Hebei Medical University, Medical experimental Center, People's Hospital of Hebei Province, Shijiazhuang, China.
Clin Exp Immunol. 2010 Oct;162(1):75-83. doi: 10.1111/j.1365-2249.2010.04226.x.
We have shown that immunization with dendritic cells (DCs) pulsed with hepatitis B virus core antigen virus-like particles (HBc-VLP) packaging with cytosine-guanine dinucleotide (CpG) (HBc-VLP/CpG) alone were able to delay melanoma growth but not able to eradicate the established tumour in mice. We tested whether, by modulating the vaccination approaches and injection times, the anti-tumour activity could be enhanced. We used a B16-HBc melanoma murine model not only to compare the efficacy of DC vaccine immunized via footpads, intravenously or via intratumoral injections in treating melanoma and priming tumour-specific immune responses, but also to observe how DC vaccination could improve the efficacy of adoptively transferred T cells to induce an enhanced anti-tumour immune response. Our results indicate that, although all vaccination approaches were able to protect mice from developing melanoma, only three intratumoral injections of DCs could induce a significant anti-tumour response. Furthermore, the combination of intratumoral DC vaccination and adoptive T cell transfer led to a more robust anti-tumour response than the use of each treatment individually by increasing CD8(+) T cells or the ratio of CD8(+) T cell/regulatory T cells in the tumour site. Moreover, the combination vaccination induced tumour-specific immune responses that led to tumour regression and protected surviving mice from tumour rechallenge, which is attributed to an increase in CD127-expressing and interferon-γ-producing CD8(+) T cells. Taken together, these results indicate that repeated intratumoral DC vaccination not only induces expansion of antigen-specific T cells against tumour-associated antigens in tumour sites, but also leads to elimination of pre-established tumours, supporting this combined approach as a potent strategy for DC-based cancer immunotherapy.
我们已经证明,用乙型肝炎病毒核心抗原病毒样颗粒(HBc-VLP)包被胞嘧啶-鸟嘌呤二核苷酸(CpG)(HBc-VLP/CpG)脉冲的树突状细胞(DC)免疫,单独使用能够延迟黑色素瘤的生长,但不能根除小鼠体内已建立的肿瘤。我们测试了通过调节疫苗接种方法和注射时间,是否可以增强抗肿瘤活性。我们使用 B16-HBc 黑色素瘤小鼠模型,不仅比较了通过足底、静脉内或肿瘤内注射接种 DC 疫苗治疗黑色素瘤和启动肿瘤特异性免疫反应的功效,还观察了 DC 疫苗接种如何提高过继转移 T 细胞的功效,以诱导增强的抗肿瘤免疫反应。我们的结果表明,虽然所有疫苗接种方法都能够保护小鼠免受黑色素瘤的发展,但只有三次肿瘤内注射 DC 才能诱导出显著的抗肿瘤反应。此外,与单独使用每种治疗方法相比,肿瘤内 DC 疫苗接种和过继 T 细胞转移的联合使用通过增加肿瘤部位的 CD8+T 细胞或 CD8+T 细胞/调节性 T 细胞的比例,导致更强大的抗肿瘤反应。此外,联合疫苗接种诱导了肿瘤特异性免疫反应,导致肿瘤消退,并保护存活的小鼠免受肿瘤再挑战,这归因于 CD127 表达和干扰素-γ产生的 CD8+T 细胞的增加。总之,这些结果表明,重复肿瘤内 DC 疫苗接种不仅诱导肿瘤部位针对肿瘤相关抗原的抗原特异性 T 细胞扩增,而且还导致已建立的肿瘤消除,支持这种联合方法作为基于 DC 的癌症免疫治疗的有效策略。