Plasticity of Immune Responses Suppressing Parasitemia During Acute Plasmodium chabaudi Malaria

Abstract

γδ T cells have a crucial role in cell-mediated immunity (CMI) against P. chabaudi malaria, but δ-chain knockout (KO) (δo/o) mice and mice depleted of γδ T cells with mAb cure this infection. To address the question of why mice deficient in γδ T cells resolve P. chabaudi infections, we immunized δo/o mice by infection with viable blood-stage parasites. Sera from infection-immunized mice were tested for their ability to protect JHo/o, δo/o double KO mice passively against P. chabaudi challenge infection. The onset of parasitemia was significantly delayed in mice receiving immune sera, compared with saline or uninfected serum controls. Immune sera were then fractionated into Ig-rich and Ig-depleted fractions by HPLC on a protein G column. Double KO mice were passively immunized with either fraction and challenged with P. chabaudi. The onset of parasitemia was significantly delayed in recipients of the Ig-rich fraction compared with recipients of the Ig-poor fraction of immune sera. We conclude that δo/o mice, which are unable to activate CMI against the parasite, suppress P. chabaudi infection by a redundant Ab-mediated process.