The H-2 Locus and Viral Leukemogenesis as Studied in Congenic Strains of Mice2
- 1 August 1968
- journal article
- research article
- Published by Oxford University Press (OUP) in JNCI Journal of the National Cancer Institute
- Vol. 41 (2) , 597-604
- https://doi.org/10.1093/jnci/41.2.597
Abstract
By the use of congenic resistant strains of mice, which differ essentially one from another only at single histocompatibility loci, the effect of histocompatibility-2 (H-2) on leukemogenesis by the BALB/ Tennant-leukemia (B/T-L) virus was investigated. Different alleles at this locus were found to predispose to both different incidences and to different rates of development of leukemia in mice challenged at 1–4 days of age. There were some discrepancies between the two measures of susceptibility (incidence and rate of development), but whether these were due to sampling error or represent a real difference is at present unknown. The most favorable allele, as measured by incidence of leukemia but not by the age at which leukemia developed, was H-2d, the allele of strain BALB/cJ in which the B/T-L virus originated. The least favorable allele by both measures, with concordance of results on two genetic backgrounds, was H-2b. Alleles H-2a and H-2k occupied intermediate positions, with H-2k probably the more resistant of the two. In crosses between congenic strains with different H-2 alleles there was no clear dominance of susceptibility or resistance. However, in a cross between two H-2k strains, the moderately susceptible B10.BR used in the congenic tests and the unrelated highly resistant C57BR/cdJ, resistance was dominant. Since both these strains are H-2k, the H-2 locus cannot be responsible for differences in susceptibility in this instance. The significance of these findings is discussed.Keywords
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