The quantity of thymus-
leukemia (
TL) antigens expressed by murine
leukemia cells is significantly greater than that expressed by somatic hybrids of such cells. Based upon the results of 125I-lactoperoxidase labeling and antibody absorption procedures, and corrected for size differences between the two cell types, the quantity of
TL antigens expressed by RADA-1 cells, a radiation-induced murine
leukemia cell line of strain A/J mice, is approximately 5.0 times greater than that of somatic hybrids of RADA-1 and LM(TK)- cells. LM(TK)- cells are a
thymidine kinase-deficient TL(-) mouse fibroblast cell line. The quantity of
TL antigens expressed is related only in part to their susceptibility to lysis by TL
antibodies and guinea pig
complement (GPC). RADA-1 cells resist lysis. The quantity of
TL antigens expressed by RADA-1 cells is analogous to that formed by nonneoplastic thymocytes obtained from F1 hybrids of two strains of TL(+) and TL(-) mice; cells from both strains are sensitive to TL antiserum and GPC. ASL-1 cells, a spontaneously occurring
leukemia cell line of A/J mice, express
TL antigens in significantly higher quantities than any of the cell types examined. Exposed to TL
antisera, the quantity of
TL antigens of ASL-1 cells, but not that of hybrid cells, gradually diminishes. ASL-1 cells convert over a 6-h period of exposure to antibody and guinea pig
complement (GPC) resistance; hybrid cells remain sensitive. However, ASL-1 cells converted to TL antibody and GPC resistance continue for a time to express
TL antigens in quantities similar to that of sensitive F1 thymocytes and resistant RADA-1 cells. RADA-1 X LM(TK)- hybrid cells, which are sensitive to TL
antibodies and GPC, express the lowest quantities of
TL antigens of any of the cell types examined. It is likely that differences in the quantities of
TL antigens expressed by different cell lines reflect genetic mechanisms controlling
TL antigen expression. The failure of TL
antisera to affect the quantities of
TL antigens expressed by hybrid cells is taken as an indication that genetic controls governing
antigen expression may be distinguished from those involved in regulating responsiveness to specific antiserum.