Susceptibility to tumors induced by polyoma virus is conferred by an endogenous mouse mammary tumor virus superantigen

Aron E. Lukacher, Yupo Ma, John P. Carroll, Sara R. Abromson-Leeman, Joseph C. Laning, Martin E. Dorf, Thomas L. Benjamin

Research output: Contribution to journalArticlepeer-review

74 Scopus citations


A dominant gene carried in certain inbred mouse strains confers susceptibility to tumors induced by polyoma virus. This gene, designated Pyvs, was defined in crosses between the highly susceptible C3H/BiDa strain and the highly resistant but H-2k-identical C57BR/cdJ strain. The resistance of C57BR/cdJ mice is overcome by irradiation, indicating an immunological basis. In F1 × C57BR/cdJ backcross mice, tumor susceptibility cosegregates with Mtv-7, a mouse mammary tumor provirus carried by the C3H/BiDa strain. This suggests that Pyvs might encode the Mtv-7 superantigen (SAG) and abrogate polyoma tumor immunosurveillance through elimination of T cells bearing specific Vβ domains. DNA typing of 110 backcross mice showed no evidence of recombination between Pyvs and Mtv-7. Strongly biased usage of Vβ6 by polyoma virus-specific CD8+ cytotoxic T lymphocytes in C57BR/cdJ mice implicates T cells bearing this Mtv-7 SAG-reactive Vβ domain as critical anti-polyoma tumor effector cells in vivo. These results indicate identity between Pyvs and Mtv-7 sag, and demonstrate a novel mechanism of inherited susceptibility to virus-induced tumors based on effects of an endogenous superantigen on the host’s T cell repertoire.

Original languageEnglish (US)
Pages (from-to)1683-1692
Number of pages10
JournalJournal of Experimental Medicine
Issue number5
StatePublished - May 1 1995

All Science Journal Classification (ASJC) codes

  • Medicine(all)


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