Abstract
The genetic control of the in vivo growth of the Moloney virus-induced BALB/c [mouse] lymphoma YC8 was studied in F1 hybrids between BALB/c and several strains differing at the MHC and/or at the level of non-H-2 genes. Parental strains of the B10 and C3Hf but not of A, BALB/c or DBA/2 backgrounds introduced a significant resistance to the growth of 102 YC8 cells (a dose able to kill 100% of BALB/c mice) in semisyngeneic hosts. This resistance appeared to be due to non-H-2 genes although a modulation of the tumor growth by genes encoded by the MHC was also evident. The study of backcrosses between susceptible BALB/c and resistant (BALB/c .times. B10.BR)F1 crosses revealed that 83% of animals developed lethal tumors after injection of 102 YC8 cells. This high frequency of tumor takes was not linked to genes of the MHC. Adult thymectomy plus sublethal irradiation was able to abrogate the resistance of (BALB/c .times. B10.BR) or (BALB/c .times. B10.RIII)F1 mice to YC8 growth. Since the injection of silica also impaired the resistance to YC8, the genetic control of resistance to C8 is probably mediated both by T cells and macrophage-like cells.