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.
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Authors | Anthony M Byers, Annette Hadley, Aron E Lukacher |
Journal | Virology
(Virology)
Vol. 358
Issue 2
Pg. 485-92
(Feb 20 2007)
ISSN: 0042-6822 [Print] United States |
PMID | 17011010
(Publication Type: Journal Article, Research Support, N.I.H., Extramural)
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Chemical References |
- Cytokines
- Membrane Glycoproteins
- Pore Forming Cytotoxic Proteins
- Tumor Necrosis Factor-alpha
- Perforin
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Topics |
- Animals
- CD8-Positive T-Lymphocytes
(immunology)
- Cells, Cultured
- Cytokines
(biosynthesis)
- Lymphocyte Count
- Membrane Glycoproteins
(deficiency, genetics)
- Mice
- Mice, Inbred C3H
- Mice, Inbred C57BL
(genetics)
- Perforin
- Polyomavirus
(immunology)
- Polyomavirus Infections
(immunology)
- Pore Forming Cytotoxic Proteins
(deficiency, genetics)
- Species Specificity
- Tumor Necrosis Factor-alpha
(biosynthesis)
- Tumor Virus Infections
(immunology)
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