Poster Presentation 28th Lorne Cancer Conference 2016

Redirecting immune subsets through genetic manipulation for enhancing adoptive immunotherapy (#283)

Carmen SM Yong 1 , Jennifer A Westwood 1 , Jan Schroder 2 3 , Anthony T Papenfuss 1 2 3 4 , Bianca von Scheidt 1 , Maria Moeller 1 , Christel Devaud 1 , Phil Darcy 1 5 , Michael Kershaw 1 5
  1. Sir Peter MacCallum Department of Oncology, The University of Melbourne, Parkville, Vic, Australia
  2. Cancer Genomics Program, Sir Peter MacCallum Department of Oncology, The University of Melbourne, Parkville, Vic, Australia
  3. Bioinformatics Division, The Walter and Eliza Hall Institute of Medical Research, Parkville, Vic, Australia
  4. Department of Medical Biology, The University of Melbourne, Parkville, Vic, Australia
  5. Department of Immunology, Monash University, Melbourne, Vic, Australia

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, Her2 (ERB). 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. We established CAR expression within multiple immune subsets, and furthermore demonstrated antigen-specific responses from CAR+ T cells in both cytokine release and cytotoxicity. In addition, upon tumour challenge, vav-CAR mice were able to mount an effective immune response upon recognition of the Her2 antigen, and this tumour rejection was dependent on Natural Killer cells and T cells. 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.