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Alloreactive cytotoxic T lymphocytes lyse syngeneic influenza-infected tumour cell targets
Spleen cells from C57BL/10(H-2b) mice, when stimulated in vitro to Kk alloantigens, lysed syngeneic influenza A virus-infected tumour cell targets but not uninfected or vaccinia- or Sendai virus-infected targets. Peritoneal macrophage targets infected with influenza virus were not lysed. Lysis of H-2k targets and EL4-A influenza virus-infected targets was abrogated by treatment of effectors with anti-Thy 1.2 plus C and anti-Lyt 2 plus C but not by anti-Lyt 1 plus C or anti-GM-1, a natural killer cell-specific, monoclonal antibody plus C. Cold target inhibition experiments indicated that one and the same population of Tc cells see H-2Kk and H-2b plus influenza virus. Sensitization of C57BL/10 mice to Kk in vivo did not potentiate virus clearance from lungs. The data are discussed in relation to observed Ir gene effects and variation and modulation of H-2 antigens on tumour cells.
Spleen cells from C57BL/10(H-2b) mice, when stimulated in vitro to Kk alloantigens, lysed syngeneic influenza A virus-infected tumour cell targets but not uninfected or vaccinia- or Sendai virus-infected targets. Peritoneal macrophage targets infected with influenza virus were not lysed. Lysis of H-2k targets and EL4-A influenza virus-infected targets was abrogated by treatment of effectors with anti-Thy 1.2 plus C and anti-Lyt 2 plus C but not by anti-Lyt 1 plus C or anti-GM-1, a natural killer cell-specific, monoclonal antibody plus C. Cold target inhibition experiments indicated that one and the same population of Tc cells see H-2Kk and H-2b plus influenza virus. Sensitization of C57BL/10 mice to Kk in vivo did not potentiate virus clearance from lungs. The data are discussed in relation to observed Ir gene effects and variation and modulation of H-2 antigens on tumour cells.