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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.

Authors:
 [1];  [1];  [2]
  1. Department of Pathology, Emory University School of Medicine, Woodruff Memorial Research Building, Rm. 7307, 101 Woodruff Circle, Atlanta, GA 30322 (United States)
  2. Department of Pathology, Emory University School of Medicine, Woodruff Memorial Research Building, Rm. 7307, 101 Woodruff Circle, Atlanta, GA 30322 (United States). E-mail: alukach@emory.edu
Publication Date:
OSTI Identifier:
20975217
Resource Type:
Journal Article
Resource Relation:
Journal Name: Virology; Journal Volume: 358; Journal Issue: 2; Other Information: DOI: 10.1016/j.virol.2006.08.044; PII: S0042-6822(06)00616-7; Copyright (c) 2006 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA)
Country of Publication:
United States
Language:
English
Subject:
60 APPLIED LIFE SCIENCES; BONE MARROW; GENES; LYMPHOKINES; MICE; NEOPLASMS; PATHOGENESIS; PHENOTYPE; POLYOMA VIRUS; RECEPTORS; SAFETY

Citation Formats

Byers, Anthony M., Hadley, Annette, and Lukacher, Aron E. Protection against polyoma virus-induced tumors is perforin-independent. United States: N. p., 2007. Web. doi:10.1016/j.virol.2006.08.044.
Byers, Anthony M., Hadley, Annette, & Lukacher, Aron E. Protection against polyoma virus-induced tumors is perforin-independent. United States. doi:10.1016/j.virol.2006.08.044.
Byers, Anthony M., Hadley, Annette, and Lukacher, Aron E. Tue . "Protection against polyoma virus-induced tumors is perforin-independent". United States. doi:10.1016/j.virol.2006.08.044.
@article{osti_20975217,
title = {Protection against polyoma virus-induced tumors is perforin-independent},
author = {Byers, Anthony M. and Hadley, Annette and Lukacher, Aron E.},
abstractNote = {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.},
doi = {10.1016/j.virol.2006.08.044},
journal = {Virology},
number = 2,
volume = 358,
place = {United States},
year = {Tue Feb 20 00:00:00 EST 2007},
month = {Tue Feb 20 00:00:00 EST 2007}
}