Please use this identifier to cite or link to this item: https://www.um.edu.mt/library/oar/handle/123456789/55101
Title: Interferon gamma induction in human melanoma cell/allogeneic leukocyte co-cultures is enhanced by interleukin 18 but drug resistant melanoma cells are poorer inducers of IFN-gamma
Authors: Micallef, Mark J.
Darmanin, Stephanie
Buhagiar, Joseph A.
Camilleri-Podesta, Marie Therese
Yamauchi, Hiroshi
Kurimoto, Masashi
Serracino-Inglott, Anthony
Ellul-Micallef, Roger
Keywords: Melanoma -- Pathophysiology
Melanoma -- Diagnosis
Melanoma -- Treatment
Cell interaction
Drug resistance in cancer cells
Immunosuppression
Doxorubicin
Issue Date: 2001
Publisher: Elsevier
Citation: Micallef, M. J., Darmanin, S., Buhagiar, J. A., Camilleri-Podesta, M. T., Yamauchi, H., Kurimoto, M., ... & Ellul-Micallef, R. (2001). Interferon gamma induction in human melanoma cell/allogeneic leukocyte co-cultures is enhanced by interleukin 18 but drug resistant melanoma cells are poorer inducers of IFN-γ. International Immunopharmacology, 1(2), 295-305.
Abstract: Human melanoma Colo 679 cells were made resistant to doxorubicin (adriamycin, ADM) by continuous exposure to ascending concentrations of the drug and Colo/ADM80; a variant which grew continuously in the presence of 80 ng/ml of ADM was thus established. Human peripheral blood mononuclear cells (PBMC) produced interferon gamma (IFN-gamma) when cultured with mitomycin C (MMC)-treated parental Colo 679 cells. The synthesis of IFN-gamma was synergistically enhanced by adding interleukin-18 (IL-18) and this was IL-12-dependent because a neutralizing antibody against IL-12 almost completely inhibited IFN-gamma production while control antibodies (Abs) were inactive. The cellular sources of IFN-gamma were found to be B cells, CD8+ T cells and CD4+ T cells as revealed by flow cytometry after double staining for surface antigens and staining for intracellular IFN-gamma. Interestingly, the resistant cell line induced much less IFN-gamma production than the parental cell line under the same co-culture conditions; however, IL-18 could still enhance the production of IFN-gamma. In conclusion, our study shows that acquired resistance to anti-cancer agents can also reduce immune responses to cancer cells. However, the immunostimulatory cytokine IL-18 could still enhance IFN-gamma production in drug resistant tumor cell-PBMC cultures indicating that such immunostimulatory agents could still be beneficial in immunotherapy for patients with recurrent drug resistant tumors.
URI: https://www.um.edu.mt/library/oar/handle/123456789/55101
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Scholarly Works - FacSciBio

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