Abstract
We recently demonstrated differential susceptibility of cells expressing viral antigen to killing by antigen-specific cytotoxic T lymphocytes (CTLs). In addition, interferon-γ (IFN-γ) has been implicated in the clearance of some viruses from tissues. We explored the role of IFN-γ in the cytotoxicity of Sendai virus-specific CTLs against virus-infected RL♂1 (T cell leukemia) or Meth A (fibrosarcoma) cells, as well as the growth of subcutaneously(s.c.) transplanted, virus-infected cells in IFN-γ+/+ or IFN-γ−/− mice of the syngeneic strain(BALB/c). Sendai virus-specific CTLs were cytotoxic against virus-infected RL♂1 cells, and s.c. transplanted, virus-infected RL♂1 cells were acutely rejected from IFN-γ+/+ or IFN-γ−/− mice. In contrast, the CTLs were inactive toward virus-infected Meth A cells, but s.c. transplanted, virus-infected Meth A cells were acutely rejected from IFN-γ+/+ but not IFN-γ−/− mice. The s.c. growth of virus-infected Meth A cells in the mutant mice was markedly inhibited by s.c. injections of IFN-γ, and the rejection from IFN-γ+/+ mice was delayed after specific elimination of macrophages by intravenous (i.v.) injections of dichloromethylene diphosphonatecontaining liposomes. These results suggest an essential role of IFN-γ and involvement of macrophage in the rejection of CTL-resistant, virus-infected cells.
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