Abstract
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.
MeSH Terms
Animals
Antigens, Neoplasm
Cell Line
Chromosome Mapping
Cytotoxicity, Immunologic
Genes, MHC Class II
Genetic Linkage
Histocompatibility
Hybridization, Genetic
Immunity, Cellular
Leukemia, Experimental/genetics,immunology
Mice
Mice, Inbred AKR
Mice, Inbred Strains
Species Specificity
Chemicals
Antigens, Neoplasm
Authors & Affiliations
3 authors, click to expand affiliations / ORCID
Meruelo D
Deak B
McDevitt H O
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