Figure 7. Course of a P. falciparum MSP1₁₉ Transgenic P. berghei Infection in Mice.

(A) Groups of 2–3 FcγRI transgenic (Tg) or nontransgenic (NTg) littermates were injected i.p. with a total dose of 1.5 mg fully human anti–P. falciparum MSP1₁₉ IgG1 (JS1), an irrelevant human IgG1 (B10) recognizing MSP1₁₉ from P. yoelii or PBS. Similar results were obtained in two independent experiments. **Only groups of mice given JS1 in the FcγRI Tg were significantly different to all the other control groups with a p < 0.01. †, death of mice.

(B) Repeat experiment in FcγRI Tr animals using a lower total dose (0.75 mg) of JS1. Coadministration of the blocking mAb 10.1 specific for the IgG1 binding site on human FcγRI abrogates the protection mediated by the passively administered JS1 antibody. Each point represents the geometric mean parasitemia of mice in each group at the time after i.p. challenge with 5,000 parasitized erythrocytes. Only those animals receiving the fully human anti–P. falciparum MSP1₁₉ IgG1 Ab in a human FcγRI background survived an otherwise lethal infection; all the mice in the other groups with high parasitemias were killed on either day 7 or 8. Similar results were obtained in two independent experiments. **Only groups of mice given JS1 in the FcγRI Tg were significantly different to all the other control groups with a p < 0.01. †, death of mice.

(C–E) ×100 magnification of Giemsa-stained smears of blood taken from control animals (C) and FcγRI Tg animals treated with JS1 (D and E). Note the presence of phagocytosed merozoites within the cytoplasm of cells displaying mononuclear morphology (arrow).