Chaput N, Conforti R, Viaud S, Spatz A, Zitvogel L
Institut Gustave Roussy (IGR), Villejuif, France.
Oncogene. 2008 Oct 6;27(45):5920-31. doi: 10.1038/onc.2008.270.
On the basis of experimental models and some human data, we can assume that tumor outgrowth results from the balance between immunosurveillance (the extrinsic tumor suppressor mechanisms) and immunosubversion dictated by transformed cells and/or the corrupted surrounding microenvironment. Cancer immunosurveillance relies mainly upon conventional lymphocytes exerting either lytic or secretory functions, whereas immunosubversion results from the activity of regulatory T or suppressor myeloid cells and soluble mediators. Although specific tools to target or ablate dendritic cells (DCs) became only recently available, accumulating evidence points to the critical role of the specialized DC system in dictating most of the conventional and regulatory functions of tumor-specific T lymphocytes. Although DC can be harnessed to silence tumor development, tumors in turn can exploit DC to evade immunity. Indeed, DCs harbor defects in their differentiation and stimulatory functions in cancer-bearing hosts and can actively promote T-cell tolerance to self-tumor antigens. In this review, we will focus on the dual role of DC during tumor progression and discuss pharmacoimmunological strategies to harness DC against cancer.
基于实验模型和一些人类数据，我们可以假设肿瘤生长源于免疫监视（外在肿瘤抑制机制）与转化细胞和/或受损周围微环境所主导的免疫颠覆之间的平衡。癌症免疫监视主要依赖于发挥溶解或分泌功能的传统淋巴细胞，而免疫颠覆则源于调节性T细胞或抑制性髓样细胞以及可溶性介质的活动。尽管靶向或消除树突状细胞（DC）的特定工具直到最近才出现，但越来越多的证据表明，专门的DC系统在决定肿瘤特异性T淋巴细胞的大多数传统和调节功能方面起着关键作用。尽管DC可被用于抑制肿瘤发展，但肿瘤反过来也可利用DC逃避免疫。事实上，在荷瘤宿主中，DC在其分化和刺激功能方面存在缺陷，并可积极促进T细胞对自身肿瘤抗原的耐受性。在这篇综述中，我们将重点关注DC在肿瘤进展过程中的双重作用，并讨论利用DC对抗癌症的药物免疫策略。
