Interaction of H-2 and non-H-2 genes in spontaneous resistance to adenocarcinoma ADK-1t in F1 mice.
The genetic control of spontaneous resistance in vivo to increasing doses of a poorly immunogenic spontaneous adenocarcinoma (ADK-1t) of BALB/c origin was studied in F1 hybrid mice. The spontaneous resistance of homozygous parental BALB/c mice was not increased in F1 hybrids of BALB/c and BALB.B or BALB.K mice, even with small tumor challenges (10(3) cells). By contrast, it was significantly enhanced in F1 hybrids of BALB/c and several strains on A or B10 background. Resistance due to the acquisition of a new set of background genes was, however, markedly enhanced or suppressed by the presence of particular alleles located within or closely linked to the H-2 complex, as demonstrated by increasing the tumor challenge to 10(4) or 10 (5) cells. Spontaneous resistance, effective even with high tumor inocula, thus depended on a complex interplay between background and H-2 genes.
D000230:Adenocarcinoma / Q000235:genetics* / Q000276:immunology; D000818:Animals; D005260:Female; D006183:H-2 Antigens; D008297:Male; D008325:Mammary Neoplasms, Experimental / Q000235:genetics* / Q000276:immunology; D051379:Mice; D008807:Mice, Inbred BALB C / Q000235:genetics; D008815:Mice, Inbred Strains / Q000235:genetics
D006183:H-2 Antigens