Protection against polyoma virus-induced tumors is perforin-independent

Anthony M. Byers; Annette Hadley; Aron E. Lukacher

doi:10.1016/j.virol.2006.08.044

Protection against polyoma virus-induced tumors is perforin-independent

Anthony M. Byers, Annette Hadley, Aron E. Lukacher

Research output: Contribution to journal › Article › peer-review

7 Scopus citations

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 language	English (US)
Pages (from-to)	485-492
Number of pages	8
Journal	Virology
Volume	358
Issue number	2
DOIs	https://doi.org/10.1016/j.virol.2006.08.044
State	Published - Feb 20 2007

All Science Journal Classification (ASJC) codes

Virology

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10.1016/j.virol.2006.08.044

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@article{3533043d11d04491a1f10c3e3a9de589,

title = "Protection against polyoma virus-induced tumors is perforin-independent",

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.",

author = "Byers, {Anthony M.} and Annette Hadley and Lukacher, {Aron E.}",

note = "Funding Information: This work was supported by National Institutes of Health Grants CA71971 and CA100644.",

year = "2007",

month = feb,

day = "20",

doi = "10.1016/j.virol.2006.08.044",

language = "English (US)",

volume = "358",

pages = "485--492",

journal = "Virology",

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publisher = "Academic Press Inc.",

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T1 - Protection against polyoma virus-induced tumors is perforin-independent

AU - Byers, Anthony M.

AU - Hadley, Annette

AU - Lukacher, Aron E.

N1 - Funding Information: This work was supported by National Institutes of Health Grants CA71971 and CA100644.

PY - 2007/2/20

Y1 - 2007/2/20

N2 - 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.

AB - 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.

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JO - Virology

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Protection against polyoma virus-induced tumors is perforin-independent

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