title: Alteration of cell-surface antigenicity of the mouse plasmacytoma. I. Immunologic characterization of surface antigens masked during successive transplantations.
abstract: Alterations of membrane antigenicity of IgA-synthesizing plasmacytoma cells (58-8) induced in a BALB/c mouse were investigated with rabbit antisera against 58-8 transplanted from 7-8 generations (anti-58-8) and mouse antisera against H-2d (anti-H-2d). The 58-8 cells transplanted (TP) for 8 generations (TP8), showed moderate susceptibilities to anti-58-8 [cytotoxicity index (CI) = 72%] and to anti-H-2d (Cl = 30-40%). At TP12, the susceptibility to anti-58-8 remained (tCl approximately 50%) but there was none to anti-H-2d (Cl = 0-10%). After TP13, 58-8 cells had detectable reactivity neither with anti-58-8 nor with anti-H-2d before proteolysis. However, antigenicity was demonstrated after treatment of cells with proteases: Anti-58-8 and anti-H-2d became cytotoxic to pronase-treated 58-8 (P-58-8) and these cytotoxic reactivities of antisera could be completely absorbed with P-58-8- but not with "intact" 58-8. Anti-H-2d absorbed with P-58-8 had no cytotoxicity to BALB/c spleen cells. Absorption of anti-H-2d with BALB/c spleen cells did not show any measurable cytotoxicity to P-58-8. Appearance of antigenicity after proteolysis was transient and reversible. When P-58-8 was incubated in vitro, susceptibilities to antisera were decreased. Actinomycin D and puromycin inhibited the loss of susceptibility; these metabolic inhibitors suppressed the "masking" of antigenic determinants with protein-like material(s). In early generations (TP8), 58-8 cells were susceptible to antiserum to bone marrow-derived lymphocytes (anti-B) and complement. The cells completely absorbed the cytotoxicity of anti-B against spleen cells. After additional transplantations (TP14, TP30), susceptibilities to anti-B were no longer detectable and no removal of the cytotoxicity was shown, though the cells were pretreated with pronase. Anti-B failed to kill MOPC-31C.
mesh_terms: D000818:Animals; D000951:Antigens, Neoplasm; D001402:B-Lymphocytes / Q000276:immunology; D001853:Bone Marrow / Q000276:immunology; D001854:Bone Marrow Cells; D002462:Cell Membrane / Q000276:immunology; D003165:Complement System Proteins; D003609:Dactinomycin / Q000494:pharmacology; D000939:Epitopes; D006649:Histocompatibility Antigens; D007070:Immunoglobulin A; D051379:Mice; D008807:Mice, Inbred BALB C; D009368:Neoplasm Transplantation; D009374:Neoplasms, Experimental / Q000276:immunology; D010447:Peptide Hydrolases / Q000494:pharmacology; D010954:Plasmacytoma / Q000276:immunology*; D011402:Pronase / Q000494:pharmacology; D011691:Puromycin / Q000494:pharmacology; D013154:Spleen / Q000276:immunology; D014184:Transplantation, Homologous
chemical_list: D000951:Antigens, Neoplasm; D000939:Epitopes; D006649:Histocompatibility Antigens; D007070:Immunoglobulin A; D003609:Dactinomycin; D011691:Puromycin; D003165:Complement System Proteins; D010447:Peptide Hydrolases; D011402:Pronase