Protection against polyoma virus-induced tumors is perforin-independent

Anthony M. Byers, Annette Hadley, Aron Lukacher

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Abstract

CD8 T cells are necessary for controlling tumors induced by mouse polyoma virus (PyV), but the effector mechanism(s) responsible have not been determined. We examined the PyV tumorigenicity in C57BL/6 mice mutated in Fas or carrying targeted disruptions in the perforin gene or in both TNF receptor type I and type II genes. Surprisingly, none of these mice developed tumors. Perforin/Fas double-deficient radiation bone marrow chimeric mice were also resistant to PyV-induced tumors. Anti-PyV CD8 T cells in perforin-deficient mice were found not to differ from wild type mice with respect to phenotype, capacity to produce cytokines or maintenance of memory T cells, indicating that perforin does not modulate the PyV-specific CD8 T cell response. In addition, virus was cleared and persisted to similar extents in wild type and perforin-deficient mice. In summary, perforin/granzyme exocytosis is not an essential effector pathway for protection against PyV infection or tumorigenesis.

Original languageEnglish (US)
Pages (from-to)485-492
Number of pages8
JournalVirology
Volume358
Issue number2
DOIs
Publication statusPublished - Feb 20 2007

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All Science Journal Classification (ASJC) codes

  • Virology
  • Infectious Diseases

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