Genetic control of cell-mediated responsiveness to an AKR tumor-associated antigen: mapping of the locus involved to the I region of the H-2 complex.
The role of H-2-linked genes in controlling resistance to murine leukemia viruses has been studied by measuring the cell-mediated immune response of F1 hybrid mice (between AKR and various C3H and C57BL/10 derived, H-2 congenic strains) to an AKR tumor cell line, BW5147. The studies have shown that the ability to generate a primary or secondary cell-mediated response to an AKR tumor cell antigenic determinant is under H-2 linked control. The locus determining CML responsiveness maps in the I-J subregion. Nonresponsiveness is associated with the H-2q/k and H-2b/k hybrid genotypes, whereas responsiveness is associated with the H-2k/k homozygous genotype. Nonresponsiveness may result from (a) dominant suppression; (b) recessive responsiveness; or (c) an alternate mechanism not yet understood. This type of control may be one of several H-2-associated mechanisms of defense against virus-induced neoplasms.
D000818:Animals; D000951:Antigens, Neoplasm; D002460:Cell Line; D002874:Chromosome Mapping; D003602:Cytotoxicity, Immunologic; D005802:Genes, MHC Class II; D008040:Genetic Linkage; D006648:Histocompatibility; D006824:Hybridization, Genetic; D007111:Immunity, Cellular; D007942:Leukemia, Experimental / Q000235:genetics / Q000276:immunology*; D051379:Mice; D008806:Mice, Inbred AKR; D008815:Mice, Inbred Strains; D013045:Species Specificity
D000951:Antigens, Neoplasm