Abstract

A-RadLV, a variant of the radiation leukemia virus, inoculated intrathymically into adult mice, causes a high frequency of leukemia in haplotypes b, f, k, d, p and j on the B10 background, whereas H-2s mice are resistant. Resistance is dominant and segregates with H-2s in the offspring of (b x s)b and (b x t2)b backcrosses. Analysis of recombinant strains revealed that resistance is associated with I-A and I-B. B10.A(5R), a recombinant of two sensitive haplotypes, was found to be resistant, suggesting intra-H-2-gene complementation. The resistance of such complementing loci was demonstrated also in the trans position by testing F1 mice bred from sensitive parents. These data are taken to suggest that I-region linked complementing loci, similar to classical Ir genes, may be involved in resistance to murine leukemia.

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