First Author | Henrichsen P | Year | 2005 |
Journal | J Virol | Volume | 79 |
Issue | 15 | Pages | 10073-6 |
PubMed ID | 16014969 | Mgi Jnum | J:100101 |
Mgi Id | MGI:3586945 | Doi | 10.1128/JVI.79.15.10073-10076.2005 |
Citation | Henrichsen P, et al. (2005) Impaired virus control and severe CD8+ T-cell-mediated immunopathology in chimeric mice deficient in gamma interferon receptor expression on both parenchymal and hematopoietic cells. J Virol 79(15):10073-6 |
abstractText | Bone marrow chimeras were used to determine the cellular target(s) for the antiviral activity of gamma interferon (IFN-gamma). 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-gamma, but expression of the relevant receptor on non-T cells could be experimentally controlled. Only when the IFN-gamma 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-gamma receptor expression on parenchymal cells in the viscera is more important for virus control than IFN-gamma receptor expression on bone marrow-derived cells. |