Figure 1

Suppression of immunity by P. chabaudi infection. (a) BALB/c mice were infected with 10⁶ P. chabaudi (AS strain) parasites by intra-peritoneal injection and the proportion of peripheral blood cells parasitized (parasitemia) was monitored by Giemsa's stain of peripheral blood smears. (b) Uninfected (squares) or P. chabaudi-infected (circles) BALB/c mice were immunized with OVA/LPS at the indicated times after infection. Three weeks after immunization, sera were analyzed for OVA-specific IgG. Data represent the mean of three mice per group ±1 standard deviation (s.d.) and are representative of two similar experiments (*p ≤ 0.05, ^#p ≤ 0.005 uninfected versus P. chabaudi-infected). (c) Spleen cells from uninfected (open bars) or P. chabaudi-infected (filled bars) BALB/c mice immunized with OVA/LPS 10 days post-infection were restimulated in vitro as indicated and supernatants assayed for levels of IFN-γ (left) and IL-5 (right) after 48 h. Uninfected, immunized animals generated OVA-specific IgG responses, but OVA and LPS administered 6 hours and 12 days after infection with P. chabaudi produced significantly reduced levels of IgG (Figure 1b). Interestingly, suppression was lower in mice immunized during increasing levels of parasite infection (parasitemia; Figure 1b, 4 days). By 21 days post-infection, infected animals had regained immune responsiveness and mounted antibody responses of a similar magnitude to those seen in uninfected controls (Figure 1b, 21 and 28 days). Production of OVA-stimulated and concanavalin A (ConA) mitogen-stimulated T-cell cytokines was reduced in cultures of splenocytes taken from mice infected with P. chabaudi 10 days before immunization (Figure 1c). Thus, as described for P. falciparum in humans, P. chabaudi infection in mice induces suppression of immune responses, although these studies reveal that, in the animal model at least, this is a highly dynamic phenomenon