Alteration of Cell-Surface Antigenicity of the Mouse Plasmacytoma. I. Immunologic Characterization of Surface Antigens Masked During Successive Transplantations

Summary

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-2^d (anti-H-2^d). 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-2^d (CI=30–40%). At TP12, the susceptibility to anti-58-8 remained (CI≈50%) but there was none to anti-H-2^d (CI = 0-10%). After TP13, 58-8 cells had detectable reactivity neither with anti-58-8 nor with anti-H-2^dbefore proteolysis. However, antigenicity was demonstrated after treatment of cells with proteases: Anti-58-8 and anti-H-2^d 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-2^d absorbed with P-58-8 had no cytotoxicity to BALB/c spleen cells. Absorption of anti-H-2^d 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.