Protection against polyoma virus-induced tumors is perforin-independent

被引:8
作者
Byers, Anthony M. [1 ]
Hadley, Annette [1 ]
Lukacher, Aron E. [1 ]
机构
[1] Emory Univ, Sch Med, Dept Pathol, Atlanta, GA 30322 USA
关键词
polyoma virus; CD8 T cell; perforin; Fas; TNF; tumor; pathogenesis;
D O I
10.1016/j.virol.2006.08.044
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
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 perform 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. (c) 2006 Elsevier Inc. All rights reserved.
引用
收藏
页码:485 / 492
页数:8
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