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.