Antigenic modulation in vitro. III. Failure to modulate H-2 antigens on several mouse tumors.
The capacity of various malignant and normal mouse cells to acquire resistance to lysis by guinea pig complement during exposure to H-2 antisera in vitro at 37 degrees C (antigenic modulation) was examined. All tumors tested, including cell lines of the TL+ leukemias RADA1, ASL1, and RLmale1, the TL- leukemia EL 4, myelomas MOPC-70A and S194, and the sarcoma Meth A, failed to modulate when incubated with multispecific or monospecific H-2 antisera up to 24 hours, even though under comparable conditions thymus-leukemia (TL) antigens and surface IgG molecules modulated within several hours. Indirect sensitization of RADA1 leukemia cells with H-2 antisera followed by antiserum against mouse IgG also failed to induce H-2 antigen modulation. Normal peritoneal cells from certain mouse strains were partially modulated with H-2D-specific or H-2K-specific and monospecific antisera within several hours, but normal thymus and lymph node cells did not modulate. Modulation of peritoneal cells occurred without a complete loss of sensitizing H-2 antibody from the cell surface and required a cobra venom factor-sensitive activity that could be restored by human complement component C3. Modulation of TL antigens in vitro had previously been shown to have similar characteristics.
D000818:Animals; D001202:Ascitic Fluid / Q000276:immunology; D003165:Complement System Proteins; D003602:Cytotoxicity, Immunologic; D006183:H-2 Antigens; D007074:Immunoglobulin G; D066298:In Vitro Techniques; D007942:Leukemia, Experimental / Q000276:immunology*; D008297:Male; D051379:Mice; D008815:Mice, Inbred Strains; D009374:Neoplasms, Experimental / Q000276:immunology*; D013601:T-Lymphocytes / Q000276:immunology*
D006183:H-2 Antigens; D007074:Immunoglobulin G; D003165:Complement System Proteins