Ho Cheng-Maw, Chen Hui-Ling, Hu Rey-Heng, Lee Po-Huang
Department of Surgery, National Taiwan University Hospital and College of Medicine, 7 Chung-Shan South Road, Taipei 100, Taiwan.
Hepatitis Research Center, National Taiwan University Hospital, Taipei, Taiwan.
Ther Adv Med Oncol. 2019 Apr 26;11:1758835919843463. doi: 10.1177/1758835919843463. eCollection 2019.
Without stringent criteria, liver transplantation for hepatocellular carcinoma (HCC) can lead to high cancer recurrence and poor prognosis in the current treatment context. Checkpoint inhibitors can lead to long survival by targeting coinhibitory pathways and promoting T-cell activity; thus, they have great potential for cancer immunotherapy. Therapeutic modulation of cosignaling pathways may shift paradigms from surgical prevention of recurrence to oncological intervention. Herein, we review the available evidence from a therapeutic perspective and focus on immune microenvironment perturbation by immunosuppressants and checkpoint inhibitors. Partial and reversible interleukin-2 signaling blockade is the mainstream strategy of immunosuppression for graft protection. Programmed cell death protein 1 (PD-1) is abundantly expressed on human liver allograft-infiltrating T-cells, which proliferate considerably after programmed death-ligand 1 (PD-L1) blockade. Clinically, checkpoint inhibitors are used in heart, liver, and kidney recipients with various cancers. Rejection can occur after checkpoint inhibitor administration through acute T-cell-mediated, antibody-mediated, or chronic allograft rejection mechanisms. Nevertheless, liver recipients may demonstrate favorable responses to treatment for HCC recurrence without rejection. Pharmacodynamically, substantial degrees of receptor occupancy can be achieved with lower doses, with favorable clinical outcomes. Manipulation of the immune microenvironment is a therapeutic niche that balances seemingly conflicting anticancer and graft protection needs. Additional translational and clinical studies emphasizing the comparative effectiveness of signaling networks within the immune microenvironment and conducting overall assessment of the immune microenvironment may aid in creating a therapeutic window and benefiting future liver recipients with HCC recurrence.
在当前治疗背景下,若没有严格的标准,肝细胞癌(HCC)肝移植会导致癌症高复发率和不良预后。检查点抑制剂可通过靶向共抑制途径和促进T细胞活性实现长期生存;因此,它们在癌症免疫治疗方面具有巨大潜力。共信号通路的治疗性调节可能会使模式从预防复发的手术方式转变为肿瘤学干预。在此,我们从治疗角度回顾现有证据,并聚焦免疫抑制剂和检查点抑制剂对免疫微环境的干扰。部分可逆的白细胞介素-2信号阻断是保护移植物免疫抑制的主流策略。程序性细胞死亡蛋白1(PD-1)在人肝移植浸润性T细胞上大量表达,在程序性死亡配体1(PD-L1)阻断后会大量增殖。临床上,检查点抑制剂用于患有各种癌症的心脏、肝脏和肾脏移植受者。使用检查点抑制剂后可能通过急性T细胞介导、抗体介导或慢性移植物排斥机制发生排斥反应。然而,肝移植受者对HCC复发治疗可能表现出良好反应而无排斥反应。在药效学上,较低剂量即可实现较高程度的受体占有率,并取得良好临床结果。免疫微环境的调控是一个治疗领域,可平衡看似相互冲突的抗癌和移植物保护需求。更多强调免疫微环境内信号网络比较有效性并对免疫微环境进行全面评估的转化和临床研究,可能有助于创造一个治疗窗口,使未来HCC复发的肝移植受者受益。