Subject(s)
Antigens, Surface , Cell Transformation, Neoplastic/ultrastructure , Neoplasms, Experimental/ultrastructure , Animals , Antibodies , Cell Membrane/immunology , Cell Membrane/ultrastructure , Cell Movement , Cytotoxicity, Immunologic , Female , Ferritins/metabolism , H-2 Antigens , Male , Mice , Mice, Inbred BALB C , Mice, Inbred C57BL , Mice, Inbred DBA , Neoplasms, Experimental/immunology , Time FactorsABSTRACT
We have investigated the minimal molecular requirements for T cell recognition of a previously described myeloma tumor (MOPC-315-EL), which reversibly alters its reactivity with T cells. Enucleation of MOPC-315 cells, either sensitive or resistant to reaction with T cells, did not alter the ability of the resulting cytoplasts to elicit or serve as targets for anti-H-2 or anti-Sendai viral cytotoxic T lymphocytes (CTL), despite the fact that there were no detectable differences in serologically defined H-2 or viral antigens on their surface. Likewise, when plasma membranes isolated from sensitive or resistant cells were tested for their ability to elicit anti-H-2 CTL, they retained the phenotype of the cells from which they were isolated. However, solubilized and partially purified H-2 antigens from both sensitive and resistant cells were able to elicit H-2-restricted anti-Sendai virus CTL when incorporated into liposomes with purified viral glycoproteins, and anti-H-2 CTL when incorporated alone into liposomes. These results suggest that a cellular surface component(s) exists that is probably not an H-2K or H-2D gene product and is responsible for the reversible variation in the reactivity of the tumor cells with T cells.
