Kreiter Sebastian, Vormehr Mathias, van de Roemer Niels, Diken Mustafa, Löwer Martin, Diekmann Jan, Boegel Sebastian, Schrörs Barbara, Vascotto Fulvia, Castle John C, Tadmor Arbel D, Schoenberger Stephen P, Huber Christoph, Türeci Özlem, Sahin Ugur
TRON - Translational Oncology at the University Medical Center of Johannes Gutenberg University, Freiligrathstrasse 12, 55131 Mainz, Germany.
Research Center for Immunotherapy (FZI), Langenbeckstrasse 1, Building 708, 55131 Mainz, Germany.
Nature. 2015 Apr 30;520(7549):692-6. doi: 10.1038/nature14426. Epub 2015 Apr 22.
Tumour-specific mutations are ideal targets for cancer immunotherapy as they lack expression in healthy tissues and can potentially be recognized as neo-antigens by the mature T-cell repertoire. Their systematic targeting by vaccine approaches, however, has been hampered by the fact that every patient's tumour possesses a unique set of mutations ('the mutanome') that must first be identified. Recently, we proposed a personalized immunotherapy approach to target the full spectrum of a patient's individual tumour-specific mutations. Here we show in three independent murine tumour models that a considerable fraction of non-synonymous cancer mutations is immunogenic and that, unexpectedly, the majority of the immunogenic mutanome is recognized by CD4(+) T cells. Vaccination with such CD4(+) immunogenic mutations confers strong antitumour activity. Encouraged by these findings, we established a process by which mutations identified by exome sequencing could be selected as vaccine targets solely through bioinformatic prioritization on the basis of their expression levels and major histocompatibility complex (MHC) class II-binding capacity for rapid production as synthetic poly-neo-epitope messenger RNA vaccines. We show that vaccination with such polytope mRNA vaccines induces potent tumour control and complete rejection of established aggressively growing tumours in mice. Moreover, we demonstrate that CD4(+) T cell neo-epitope vaccination reshapes the tumour microenvironment and induces cytotoxic T lymphocyte responses against an independent immunodominant antigen in mice, indicating orchestration of antigen spread. Finally, we demonstrate an abundance of mutations predicted to bind to MHC class II in human cancers as well by employing the same predictive algorithm on corresponding human cancer types. Thus, the tailored immunotherapy approach introduced here may be regarded as a universally applicable blueprint for comprehensive exploitation of the substantial neo-epitope target repertoire of cancers, enabling the effective targeting of every patient's tumour with vaccines produced 'just in time'.
肿瘤特异性突变是癌症免疫治疗的理想靶点,因为它们在健康组织中不表达,并且有可能被成熟的T细胞库识别为新抗原。然而,通过疫苗方法对其进行系统性靶向一直受到阻碍,因为每个患者的肿瘤都具有一组独特的突变(“突变组”),必须首先对其进行鉴定。最近,我们提出了一种个性化免疫治疗方法,以靶向患者个体肿瘤特异性突变的全谱。在这里,我们在三个独立的小鼠肿瘤模型中表明,相当一部分非同义癌症突变具有免疫原性,而且出乎意料的是,大多数具有免疫原性的突变组被CD4(+) T细胞识别。用这种CD4(+)免疫原性突变进行疫苗接种可赋予强大的抗肿瘤活性。受这些发现的鼓舞,我们建立了一个过程,通过该过程,仅基于外显子组测序鉴定出的突变,就可以根据其表达水平和主要组织相容性复合体(MHC)II类结合能力,通过生物信息学优先排序选择作为疫苗靶点,以便快速生产合成多新表位信使RNA疫苗。我们表明,用这种多表位mRNA疫苗进行疫苗接种可诱导有效的肿瘤控制,并使小鼠体内已建立的侵袭性生长肿瘤完全消退。此外,我们证明,CD4(+) T细胞新表位疫苗接种可重塑肿瘤微环境,并诱导小鼠针对一种独立的免疫显性抗原产生细胞毒性T淋巴细胞反应,表明抗原传播的协调作用。最后,我们通过对相应人类癌症类型采用相同的预测算法,证明了人类癌症中预测与MHC II类结合的突变也很多。因此,这里介绍的定制免疫治疗方法可被视为全面利用癌症大量新表位靶点库的普遍适用蓝图,能够“及时”生产疫苗有效靶向每个患者的肿瘤。