ENDOGENOUS GAMMA-INTERFERON-INDEPENDENT HOST-RESISTANCE AGAINST LISTERIA-MONOCYTOGENES INFECTION IN CD4+ T-CELL-DEPLETED AND ASIALO GM1+ CELL-DEPLETED MICE

The effects of in vivo administration of antibodies against T-cell subsets and asialo GM1 (ASGM1)-bearing cells on endogenous gamma interferon (IFN-gamma) production and host defense in Listeria monocytogenes-infected mice were investigated. Endogenous IFN-gamma titers in the bloodstreams and spleen extracts of mice on day 2 of infection were partially suppressed by administration of rabbit anti-ASGM1 antibody, but not by anti-CD4 monoclonal antibody (MAb) or anti-CD8 MAb. Of the different combinations of these three antibodies, the most suppressive effect on IFN-gamma production was observed after administration of anti-CD4 MAb and anti-ASGM1 antibody, although anti-CD8 MAb combined with anti-CD4 MAb partially inhibited IFN-gamma production. In contrast, antilisterial resistance was suppressed by the administration of anti-CD8 MAb but not by anti-CD4 MAb or anti-ASGM1 antibody. Antilisterial resistance in mice in which both CD4+ cells and ASGM1+ cells had been depleted was performed as efficiently as in normal mice in spite of the fact that endogenous IFN-gamma production was markedly suppressed. Furthermore, these mice also eliminated L. monocytogenes cells efficiently from the spleens even when they were pretreated with anti-mouse IFN-gamma MAb. These results indicate that CD4+ T cells, CD8+ T cells, and ASGM1+ cells are all responsible for endogenous IFN-gamma production and that antilisterial resistance and endogenous IFN-gamma production are not absolutely correlated.