Fischer Cornelia, Munks Michael W, Hill Ann B, Kroczek Richard A, Bissinger Stefan, Brand Verena, Schmittnaegel Martina, Imhof-Jung Sabine, Hoffmann Eike, Herting Frank, Klein Christian, Knoetgen Hendrik
Large Molecule Research, Roche Innovation Center Munich , Penzberg, Germany.
Department of Molecular Microbiology and Immunology, Oregon Health & Science University , Portland, OR, USA.
MAbs. 2020 Jan-Dec;12(1):1834818. doi: 10.1080/19420862.2020.1834818.
Simulating a viral infection in tumor cells is an attractive concept to eliminate tumor cells. We previously reported the molecular design and the in vitro potency of recombinant monoclonal antibodies fused to a virus-derived peptide MHC class I complex that bypass the peptide processing and MHC loading pathway and directly displays a viral peptide in an MHC class I complex on the tumor cell surface. Here, we show that a vaccination-induced single peptide-specific CD8 T cell response was sufficient to eliminate B16 melanoma tumor cells in vivo in a fully immunocompetent, syngeneic mouse tumor model when mice were treated with mouse pMHCI-IgGs fusion proteins targeting the mouse fibroblast activation protein. Tumor growth of small, established B16 lung metastases could be controlled. The pMHCI-IgG had similar potency as an analogous pan-CD3 T-cell bispecific antibody. In contrast to growth control of small tumors, none of the compounds controlled larger solid tumors of MC38 cancer cells, despite penetration of pMHCI-IgGs into the tumor tissue and clear attraction and activation of antigen-specific CD8 T cells inside the tumor. pMHCI-IgG can have a similar potency as classical pan-T-cell recruiting molecules. The results also highlight the need to better understand immune suppression in advanced solid tumors.
在肿瘤细胞中模拟病毒感染是一种消除肿瘤细胞的诱人概念。我们之前报道了与病毒衍生肽MHC I类复合物融合的重组单克隆抗体的分子设计及其体外效力,该复合物绕过了肽加工和MHC加载途径,并直接在肿瘤细胞表面的MHC I类复合物中展示病毒肽。在此,我们表明,当用靶向小鼠成纤维细胞活化蛋白的小鼠pMHCI-IgG融合蛋白处理小鼠时,在完全免疫 competent 的同基因小鼠肿瘤模型中,疫苗诱导的单肽特异性CD8 T细胞反应足以在体内消除B16黑色素瘤肿瘤细胞。小的、已形成的B16肺转移瘤的肿瘤生长可以得到控制。pMHCI-IgG的效力与类似的泛CD3 T细胞双特异性抗体相似。与小肿瘤的生长控制相反,尽管pMHCI-IgG能够渗透到肿瘤组织中,并在肿瘤内部明显吸引和激活抗原特异性CD8 T细胞,但没有一种化合物能够控制MC38癌细胞的较大实体瘤。pMHCI-IgG可以具有与经典的泛T细胞招募分子相似的效力。这些结果还突出了更好地理解晚期实体瘤中免疫抑制的必要性。