Center for Cancer Immune Therapy (CCIT), Department of Hematology, Copenhagen University Hospital, Herlev, Denmark.
Symphogen A/S, Ballerup, Denmark.
Semin Immunopathol. 2017 Apr;39(3):307-316. doi: 10.1007/s00281-016-0592-y. Epub 2016 Sep 16.
Though present in low numbers, dendritic cells (DCs) are recognized as major players in the control of cancer by adaptive immunity. The roles of cytotoxic CD8 T-cells and Th1 helper CD4 T-cells are well-documented in murine models of cancer and associated with a profound prognostic impact when infiltrating human tumors, but less information is known about how these T-cells gain access to the tumor or how they are primed to become tumor-specific. Here, we highlight recent findings that demonstrate a vital role of CD103 DCs, which have been shown to be experts in cross-priming and the induction of anti-tumor immunity. We also focus on two different mediators that impair the function of tumor-associated DCs: prostaglandin E and β-catenin. Both of these mediators seem to be important for the exclusion of T-cells in the tumor microenvironment and may represent key pathways to target in optimized treatment regimens against cancer.
虽然数量较少，但树突状细胞（DC）被认为是适应性免疫控制癌症的主要参与者。细胞毒性 CD8 T 细胞和 Th1 辅助 CD4 T 细胞的作用在癌症的小鼠模型中得到了很好的证明，并与浸润人类肿瘤时的深远预后影响相关，但关于这些 T 细胞如何获得进入肿瘤的途径或它们如何被激活以成为肿瘤特异性的信息知之甚少。在这里，我们强调了最近的发现，这些发现表明 CD103 DC 具有重要作用，它们已被证明是交叉呈递和诱导抗肿瘤免疫的专家。我们还关注了两种不同的介质，它们会损害肿瘤相关 DC 的功能：前列腺素 E 和 β-连环蛋白。这两种介质似乎对于排除肿瘤微环境中的 T 细胞都很重要，并且可能是针对癌症优化治疗方案的关键途径。
