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Journal of Virology, August 2005, p. 10073-10076, Vol. 79, No. 15
0022-538X/05/$08.00+0 doi:10.1128/JVI.79.15.10073-10076.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.
Institute of Medical Microbiology and Immunology, University of Copenhagen, Copenhagen, Denmark
Received 10 January 2005/ Accepted 15 April 2005
Bone marrow chimeras were used to determine the cellular target(s) for the antiviral activity of gamma interferon (IFN-
). By transfusing such mice with high numbers of naive virus-specific CD8+ T cells, a system was created in which the majority of virus-specific CD8+ T cells would be capable of responding to IFN-
, but expression of the relevant receptor on non-T cells could be experimentally controlled. Only when the IFN-
receptor is absent on both radioresistant parenchymal and bone marrow-derived cells will chimeric mice challenged with a highly invasive, noncytolytic virus completely lack the ability to control the infection and develop severe wasting disease. Further, the study shows that IFN-
receptor expression on parenchymal cells in the viscera is more important for virus control than IFN-
receptor expression on bone marrow-derived cells.
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