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The role of Fas ligand (FasL) in programmed cell death via interaction with its receptor Fas is well characterized. It has been proposed that expression of FasL can confer immune privilege to some organs, allowing them to kill infiltrating lymphocytes and inflammatory cells. However, a number of studies have shown that when tumors or transplants express FasL, rejection often occurs as a consequence of proinflammatory functions of FasL. Here we demonstrate that FasL elicits tumor immunity in a murine melanoma model with weak immunogenicity and low expression of major histocompatibility complex (MHC) class I. We show that protected mice recognize melanocyte differentiation self-antigens. Importantly, tumor immunity is mediated by antibodies, as it can be transferred by serum from protected mice.

Original publication




Journal article


Cancer cell

Publication Date





315 - 322


MRC Human Immunology Unit and Nuffield Department of Medicine, Institute of Molecular Medicine, OX3 9DS, Oxford, United Kingdom.


Dendritic Cells, T-Lymphocytes, Lymphocytes, Tumor-Infiltrating, Tumor Cells, Cultured, Melanocytes, Bone Marrow, Animals, Mice, Inbred C57BL, Mice, Melanoma, Experimental, Lipopolysaccharides, Immunoglobulins, Membrane Glycoproteins, Luminescent Proteins, Green Fluorescent Proteins, Antibodies, Neoplasm, Autoantigens, Disease-Free Survival, Flow Cytometry, Transfection, Cell Division, Cell Differentiation, Cytotoxicity, Immunologic, Immune Tolerance, Fas Ligand Protein