Drake Charles G
Oncology, Immunology, and Urology, Johns Hopkins Sidney Kimmel Comprehensive Cancer Center, Baltimore, MD 21231, USA.
Urol Oncol. 2006 Sep-Oct;24(5):413-8. doi: 10.1016/j.urolonc.2005.08.013.
The immune response to evolving prostate cancer is a complex and carefully orchestrated process. Such a response is initiated when immature dendritic cells take up and process tumor-associated antigens. These dendritic cells must then be activated in order to present peptides to helper (CD4) T cells. Cytolytic (CD8) T cells are next "licensed" to achieve full effector function by interacting with both antigen presenting cells and tumor-specific CD4 T cells. Finally, activated CD8 T cells traffic to sites of neoplasia and mediate killing by multiple mechanisms. This article provides a basic overview of these processes, and discusses the manner by which current clinical interventions seek to augment or initiate an antitumor immune response. Various compensatory mechanisms which serve to down-regulate an antitumor response are also examined.
针对不断演变的前列腺癌的免疫反应是一个复杂且精心编排的过程。当未成熟的树突状细胞摄取并处理肿瘤相关抗原时,这样的反应就会启动。然后这些树突状细胞必须被激活,以便将肽呈递给辅助性(CD4)T细胞。接下来,细胞毒性(CD8)T细胞通过与抗原呈递细胞和肿瘤特异性CD4 T细胞相互作用而被“许可”以实现完全效应功能。最后,活化的CD8 T细胞迁移至肿瘤部位并通过多种机制介导杀伤作用。本文提供了这些过程的基本概述,并讨论了当前临床干预措施试图增强或启动抗肿瘤免疫反应的方式。还研究了用于下调抗肿瘤反应的各种补偿机制。