HPD Research Day | February 16, 2018

67 channels for fluid-tear exchange. Conclusion. Concisely, treatment of persistent epithelial defects with day and night PROSE wear should be considered when other conventional therapies have failed. Atrium – Poster 77 12:15-1:15 p.m. Modeling Melanoma-Induced Monocyte Conversion to Myeloid-Derived Suppressor Cells to Identify Novel Immunotherapies Regina Zambrano, OMS-I, Dr. Kiran C. Patel College of Osteopathic Medicine, Nova Southeastern University Julia James, D.Phil, Dr. Kiran C. Patel College of Osteopathic Medicine, Nova Southeastern University Andreas Lundqvist, Ph.D., Clinical Associate Professor, College of Allopathic Medicine, Nova Southeastern University Shannon Murray, Ph.D., Assistant Professor, College of Allopathic Medicine, Nova Southeastern University Background. Tumors have the capacity to suppress the host immune system. Tumors secrete factors that induce the conversion of CD14+ monocytes to an immunosuppressive population of cells called myeloid-derived suppressor cells (MDSC). MDSC suppress vital immune cells such as T cells by limiting their proliferation and effector cytokine production. Heightened MDSC levels in the blood and tumor microenvironment (TME) correlate to cancer, including melanoma, progression. Methods. We will use a ‘tumor education’ co-culture to model the conversion of CD14+ monocytes to MDSC upon interaction with patient-derived melanoma cells to reflect that which occurs in vivo. We will quantify these ‘melanoma-educated’ MDSC by flow cytometry using markers CD11b, HLA-DR, and CD33 to distinguish MDSC from CD14+ monocytes. MDSC suppressive effects on T cell proliferation will be measured by carboxyfluorescein succinimidyl ester (CFSE), and interferon gamma production, by enzyme-linked immunosorbent assay (ELISA). Results. We expect an increase in the conversion of CD14+ cells to MDSCs in the presence of melanoma cells as well as a decrease in T cell proliferation and IFN-gamma production upon co-culture with MDSC generated in this model. Conclusion. By developing this platform to dissect the mechanisms of MDSC generation with melanoma we will be able to identify potential therapeutic interventions to decrease MDSC generation and enhance anti-cancer immunity. With the importance of developing combination cancer immunotherapies that improve T cell responses and decrease MDSC, this tractable model will facilitate this research. Grants. This study was partially funded by an NSU President’s Faculty Development Grant to Shannon Murray.