Humoral immunity to Plasmodium berghei infection of F1 hybrid B6D2 (C57Bl/6 × DBA/2) mice was investigated using an immune serum prepared from mice which survived a lethal challenge of erythrocytic stage P. berghei because of previous vaccination with formalin-killed P. berghei. Immune serum, but not normal serum, if injected intraperitoneally or intravenously soon after infection, during rapidly increasing parasitemia, transiently inhibited the progress of infection in a pattern which was directly related to the dose and timing of serum injection. However, the level of restriction of parasitemia caused by the intravenous injection of 1 ml of immune serum could not be improved upon by subsequent additional 1-ml injections of the same serum, and parasitemia in all mice, whether delayed by immune serum or not, ultimately progressed to death. The protective capacity of the immune serum was markedly specific for plasmodial species but absorption with formalin-killed homologous parasites failed to remove the protective component. No variants of P. berghei insensitive to inhibition by immune serum were detected. The results support the view that humoral immunity to P. berghei may be mediated by more than one soluble factor and effected through at least two different pathways.
Present address: W. Alton Jones Cell Science Center, Lake Placid, New York 12946.