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.

Abstract

The role of H-2 linked genes in controlling resistance to murine leukemia viruses was 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 [leukemia] cell line, BW5147. 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 [cell mediated lympholysis] 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 dominant suppression, recessive responsiveness or 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.