The capability of the immune system for self-recognition has recently become the focus of interest for a broadening research community due to the impressive clinical results achieved with immune checkpoint inhibitors and other immunotherapies in the treatment of advanced metastatic carcinoma [1]. A significant portion of this clinical efficacy is attributed to the fact that the genomic instability of cancer generates mutation-derived peptides (neopeptides) that are not present in normal cells. A subset of these neopeptides may be neoantigens (also called neoepitopes) which are recognized as alien by cytotoxic T cells. Ideally, a cell producing neoantigens should be eliminated by the immune system. However, tumors are able to inhibit this immune response by activating various checkpoint mechanisms; these can be overcome by the now widely used therapeutic agents of checkpoint inhibitors such as anti PD-L1 or anti-CTLA-4 antibodies. There is increasing evidence that such neoantigen-driven immune responses are responsible for the significant clinical response shown to immune checkpoint inhibitors in at least one specific type of tumors, microsatellite instable cancer [2, 3].

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新抗原的计算预测：我们是否需要更多数据或新方法？

由于免疫检查点抑制剂和其他免疫疗法在晚期转移性癌的治疗中取得了令人印象深刻的临床结果，免疫系统的自我识别能力最近已成为广泛研究领域关注的焦点[1]。这种临床功效的很大一部分归因于以下事实：癌症的基因组不稳定性会产生正常细胞中不存在的突变衍生肽（新肽）。这些新肽的一个子集可能是被细胞毒性T细胞识别为外源的新抗原（也称为新表位）。理想情况下，应通过免疫系统消除产生新抗原的细胞。但是，肿瘤能够通过激活各种检查点机制来抑制这种免疫反应。这些可以通过现在广泛使用的检查点抑制剂的治疗剂来克服，例如抗PD-L1或抗CTLA-4抗体。越来越多的证据表明，这种新抗原驱动的免疫反应是对至少一种特定类型的肿瘤（微卫星不稳定的癌症）中免疫检查点抑制剂的重要临床反应的原因[2，3]。