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首页> 外文期刊>Molecular cancer therapeutics >Characterization of the CCL21-mediated melanoma-specific immune responses and in situ melanoma eradication.
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Characterization of the CCL21-mediated melanoma-specific immune responses and in situ melanoma eradication.

机译：CCL21介导的黑色素瘤特异性免疫反应和原位黑色素瘤根除的表征。

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Previous studies have shown that secondary lymphoid chemokine, CCL21, can be used for modulation of tumor-specific immune responses. Here, using B16F0 melanoma cells stably expressing CCL21 under the control of cytomegalovirus and ubiquitin promoters, we showed that CCL21-activated immune responses depend on the amount of melanoma-derived chemokine, which, in turn, depends on the strength of the promoter. We showed that ubiquitin promoter-driven expression of CCL21 enabled massive infiltration of tumors with CD4(+)CD25(-), CD8(+) T lymphocytes, and CD11c(+) dendritic cells, and consequent activation of cellular and humoral immune responses sufficient for complete rejection of CCL21-positive melanomas within 3 weeks in all tumor-inoculated mice. Mice that rejected CCL21-positive tumors acquired protective immunity against melanoma, which was transferable to naive mice via splenocytes and central memory T cells. Moreover, melanoma-derived CCL21 facilitated immune-mediated remission of preestablished, distant wild-type melanomas. Overall, these results suggest that elevated levels of tumor-derived CCL21 are required for the activation of strong melanoma-specific immune responses and generation of protective immunologic memory. They also open new perspectives for the development of novel vaccination strategies against melanoma, which use intratumoral delivery of the optimized CCL21-encoding vectors in conjunction with DNA-based vaccines.
机译：先前的研究表明，次级淋巴趋化因子CCL21可用于调节肿瘤特异性免疫反应。在这里，使用在巨细胞病毒和泛素启动子的控制下稳定表达CCL21的B16F0黑色素瘤细胞，我们显示CCL21激活的免疫反应取决于黑色素瘤衍生的趋化因子的量，而趋化因子的数量又取决于启动子的强度。我们显示泛素启动子驱动的CCL21表达使CD4（+）CD25（-），CD8（+）T淋巴细胞和CD11c（+）树突状细胞大量浸润，并因此激活了足够的细胞和体液免疫应答在所有肿瘤接种的小鼠中，在3周内完全排除了CCL21阳性黑色素瘤。拒绝CCL21阳性肿瘤的小鼠获得了针对黑色素瘤的保护性免疫力，该免疫力可通过脾细胞和中央记忆T细胞转移至幼稚小鼠。此外，源自黑素瘤的CCL21促进了预先建立的，远距离的野生型黑素瘤的免疫介导缓解。总体而言，这些结果表明，激活强烈的黑色素瘤特异性免疫反应和产生保护性免疫记忆需要高水平的肿瘤来源的CCL21。他们还为开发针对黑色素瘤的新型疫苗接种策略开辟了新的前景，该策略使用肿瘤内递送优化的CCL21编码载体和基于DNA的疫苗。

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