Department of Biological Sciences, University of Southampton, Southampton, United Kingdom; Institute for Life Sciences, University of Southampton, Southampton, United Kingdom
Department of Biological Sciences, University of Southampton, Southampton, United Kingdom; Institute for Life Sciences, University of Southampton, Southampton, United Kingdom
Cesar Tovar
Menzies Institute for Medical Research, University of Tasmania, Hobart, Australia
Institute for Life Sciences, University of Southampton, Southampton, United Kingdom; Centre for Cancer Immunology, Faculty of Medicine, University of Southampton, Southampton, United Kingdom
Jim Kaufman
Department of Veterinary Medicine, University of Cambridge, Cambridge, United Kingdom; Department of Pathology, University of Cambridge, Cambridge, United Kingdom
Tim Elliott
Institute for Life Sciences, University of Southampton, Southampton, United Kingdom; Centre for Cancer Immunology, Faculty of Medicine, University of Southampton, Southampton, United Kingdom
Department of Biological Sciences, University of Southampton, Southampton, United Kingdom; Institute for Life Sciences, University of Southampton, Southampton, United Kingdom
Devil Facial Tumour 2 (DFT2) is a recently discovered contagious cancer circulating in the Tasmanian devil (Sarcophilus harrisii), a species which already harbours a more widespread contagious cancer, Devil Facial Tumour 1 (DFT1). Here we show that in contrast to DFT1, DFT2 cells express major histocompatibility complex (MHC) class I molecules, demonstrating that loss of MHC is not necessary for the emergence of a contagious cancer. However, the most highly expressed MHC class I alleles in DFT2 cells are common among host devils or non-polymorphic, reducing immunogenicity in a population sharing these alleles. In parallel, MHC class I loss is emerging in vivo, thus DFT2 may be mimicking the evolutionary trajectory of DFT1. Based on these results we propose that contagious cancers may exploit partial histocompatibility between the tumour and host, but that loss of allogeneic antigens could facilitate widespread transmission of DFT2.