INTERFERON-GAMMA AND THE INDUCTION OF PROTECTIVE IGG2A ANTIBODIES IN NONLETHAL PLASMODIUM-BERGHEI INFECTIONS OF MICE

Mice treated with anti-IFN-gamma monoclonal antibodies were unable to recover from infection with an attenuated variant of P. berghei (Pb XA T) which causes non-lethal malaria in normal mice. On the other hand, treatment with anti-Il-4 monoclonal antibodies had no effect on the co urse of infection. IFN-gamma was produced by spleen cells in vitro dur ing the early phase of the infection. Treatment with anti-IFN-gamma su ppressed development of an anti-plasmodial IgG2a immunoglobulin isotyp e in the serum of infected mice whereas anti-IL-4 interfered with the IgG1 response. An IgG2a fraction of immune serum collected from mice t hat had recovered from Pb XAT transferred immunity to naive mice but t he IgG1 fraction did not. When glutaraldehyde fixed parasitized erythr ocytes were incubated with immune serum in suspension, specific IgG2a antibodies were detected by fluorescein staining on the membranes of c ells infected with mature stages of parasites. These results indicate that IFN-gamma is a key to inducing B cells to produce the protective antiplasmodial IgG2a immunoglobulin isotype. Antibody-dependent cell-m ediated parasite killing seems to be involved in the mechanism of reco very from infection with Pb XAT.