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Interferon‐gamma and the induction of protective lgG2a antibodies in non‐lethal 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 XAT) which causes non‐lethal malaria in normal mice. On the other hand, treatment with anti‐lL‐4 monoclonal antibodies had no effect on the course of infection. IFN‐gamma was produced by spleen cells in vitro during the early phase of the infection. Treatment with anti‐IFN‐gamma suppressed development of an anti‐plasmodial IgG2a immunoglobulin isotype in the serum of infected mice whereas anti‐IL‐4 interfered with the IgGl response. An lgG2a fraction of immune serum collected from mice that had recovered from Pb XA T transferred immunity to naive mice but the IgGl fraction did not. When glutaraldehyde fixed parasitized erythrocytes were incubated with immune serum in suspension, specific IgG2a antibodies were detected by fluorescein staining on the membranes of cells infected with mature stages of parasites. These results indicate that IFN‐gamma is a key to inducing B cells to produce the protective anti‐plasmodial IgG2a immunoglobulin isotype. Antibody‐dependent cell‐mediated parasite killing seems to be involved in the mechanism of recovery from infection with Pb XAT.