Endogenous gamma interferon-independent host resistance against Listeria monocytogenes infection in CD4⁺ T cell- 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-γ) production and host defense in Listeria monocytogenes-infected mice were investigated. Endogenous IFN-γ 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-γ 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-γ 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-γ 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-γ MAb. These results indicate that CD4⁺ T cells, CD8⁺ T cells, and ASGM1⁺ cells are all responsible for endogenous IFN-γ production and that antilisterial resistance and endogenous IFN-γ production are not absolutely correlated.