Abstract
The murine 402AX teratocarcinoma is an H-2 negative, nullipotent stem cell tumor of testicular origin. Previous studies have demonstrated that host strain resistance and susceptibility to this tumor are under the control of 2 genes, one of which is closely linked to the mouse major histocompatibility complex. Earlier studies determined the lack of antigenic modulation and the absence of H-2 antigens on 402AX cells passaged in vitro or in genetically susceptible hosts. The present studies demonstrate that when passaged in genetically resistant host mice [C57BL/10, B10.SM, and B10.129(6M)], the H-2 negative 402AX cells modulate to become positive for H-2b antigens, as detected by indirect immunofluorescence, microcytotoxicity, and quantitative absorption. Two to 4 days of in vivo growth in resistant hosts is necessary for H-2b antigens to be expressed. H-2 positive tumor cells removed from resistant hosts and placed in culture become H-2 antigen negative within 1 to 4 hr in vitro. H-2 antigen turn-on on the teratocarcinoma cells is specific for the H-2 haplotype of the tumor cell origin (129, H-2b); alien H-2 antigens are not expressed. The observation that only teratocarcinoma cells growing in genetically resistant hosts turn-on for H-2 antigens suggests that major histocompatibility antigens on target cells are required for an efficient host cell-mediated immune response against tumor cells.
