Yong Carmen S M, Westwood Jennifer A, Schröder Jan, Papenfuss Anthony T, von Scheidt Bianca, Moeller Maria, Devaud Christel, Darcy Phillip K, Kershaw Michael H
Sir Peter MacCallum Department of Oncology, University of Melbourne, Parkville, Victoria 3010, Australia.
Bioinformatics Division, The Walter & Eliza Hall Institute of Medical Research, Parkville, Victoria, 3052, Australia; Bioinformatics and Cancer Genomics, Peter MacCallum Cancer Centre, East Melbourne, Victoria, 3002, Australia; Department of Computing and Information Systems, The University of Melbourne, Parkville, Victoria, 3010, Australia.
PLoS One. 2015 Oct 27;10(10):e0140543. doi: 10.1371/journal.pone.0140543. eCollection 2015.
Genetically modified CD8+ T lymphocytes have shown significant anti-tumor effects in the adoptive immunotherapy of cancer, with recent studies highlighting a potential role for a combination of other immune subsets to enhance these results. However, limitations in present genetic modification techniques impose difficulties in our ability to fully explore the potential of various T cell subsets and assess the potential of other leukocytes armed with chimeric antigen receptors (CARs). To address this issue, we generated a transgenic mouse model using a pan-hematopoietic promoter (vav) to drive the expression of a CAR specific for a tumor antigen. Here we present a characterization of the immune cell compartment in two unique vav-CAR transgenic mice models, Founder 9 (F9) and Founder 38 (F38). We demonstrate the vav promoter is indeed capable of driving the expression of a CAR in cells from both myeloid and lymphoid lineage, however the highest level of expression was observed in T lymphocytes from F38 mice. Lymphoid organs in vav-CAR mice were smaller and had reduced cell numbers compared to the wild type (WT) controls. Furthermore, the immune composition of F9 mice differed greatly with a significant reduction in lymphocytes found in the thymus, lymph node and spleen of these mice. To gain insight into the altered immune phenotype of F9 mice, we determined the chromosomal integration site of the transgene in both mouse strains using whole genome sequencing (WGS). We demonstrated that compared to the 7 copies found in F38 mice, F9 mice harbored almost 270 copies. These novel vav-CAR models provide a ready source of CAR expressing myeloid and lymphoid cells and will aid in facilitating future experiments to delineate the role for other leukocytes for adoptive immunotherapy against cancer.
基因改造的CD8+ T淋巴细胞在癌症的过继性免疫治疗中已显示出显著的抗肿瘤作用,最近的研究强调了其他免疫亚群组合在增强这些结果方面的潜在作用。然而,目前基因改造技术的局限性使我们难以充分探索各种T细胞亚群的潜力,也难以评估配备嵌合抗原受体(CAR)的其他白细胞的潜力。为了解决这个问题,我们使用全造血启动子(vav)构建了一个转基因小鼠模型,以驱动肿瘤抗原特异性CAR的表达。在此,我们展示了对两种独特的vav-CAR转基因小鼠模型(创始人9号(F9)和创始人38号(F38))免疫细胞区室的特征分析。我们证明vav启动子确实能够驱动CAR在髓系和淋巴系细胞中表达,然而在F38小鼠的T淋巴细胞中观察到最高水平的表达。与野生型(WT)对照相比,vav-CAR小鼠的淋巴器官更小且细胞数量减少。此外,F9小鼠的免疫组成差异很大,这些小鼠的胸腺、淋巴结和脾脏中的淋巴细胞显著减少。为了深入了解F9小鼠改变的免疫表型,我们使用全基因组测序(WGS)确定了两种小鼠品系中转基因的染色体整合位点。我们证明,与F38小鼠中发现的7个拷贝相比,F9小鼠含有近270个拷贝。这些新型vav-CAR模型提供了表达CAR的髓系和淋巴系细胞的现成来源,并将有助于推动未来的实验,以阐明其他白细胞在癌症过继性免疫治疗中的作用。