Poster Presentation 29th Lorne Cancer Conference 2017

Immune escape in primary melanoma (#120)

Andreas Behren 1 2 , Sabrina Paessler 3 , Siddhartha Deb 4 , Jonathan Cebon 4 5 , Oliver Klein 4
  1. Olivia Newton-John Cancer Research Institute, Heidelberg, VIC, Australia
  2. School of Cancer Medicine, La Trobe University, Heidelberg, VIC, Australia
  3. Department of Medical Engineering and Biotechnology, University of Applied Sciences Jena, Jena, Germany
  4. Cancer-Immunobiology, Olivia Newton-John Cancer Research Institute, Heidelberg, VIC, Australia
  5. School of Cancer Medicine, LaTrobe University, Melbourne, VIC, Australia

Tumour infiltrating lymphocytes are prognostic in all stages of melanoma and may also predict as part of an inflamed tumour microenvironment for a response to immunotherapeutic interventions. Melanoma cells can escape the antitumour immune response either by immunoselection or immunosuppression, and it is currently not well understood if both processes are mutually exclusive or not. In immune selection, melanoma cells hide from the recognition of CD8+ T lymphocytes via down-regulation and loss of melanoma specific antigens or components of the HLA class I complex. Alternatively, melanoma cells can escape anti-tumour immune responses by the expression of molecules or immunosuppressive cytokines that inhibit the cytotoxic potential of melanoma-specific T cells by engaging co-inhibitory receptors on their cell surface. One of these molecules, the programmed cell death ligand-L1, PD-L1 has been recognized as an important therapeutic target with monoclonal antibodies blocking the PD-1/PD-L1 interaction demonstrating significant clinical activity in patients with advanced melanoma. The immune escape mechanisms of melanoma in early stages of the tumour development are currently not well defined. It can be predicted that anti-melanoma immunity is shaped at the initial encounter of the tumour and the host immune system and that this interaction may influence the further disease course and potentially the responsiveness to immunotherapy. Here, we defined the immune microenvironment in early stages of melanoma with a particular focus to discriminate immunoselection and immunoevasion by investigating the expression of PD-L1, HLA-class I and lymphocyte subset infiltration using multi-colour immunofluorescence in a cohort of primary melanomas.