Advances in transcriptomics and proteomics have revealed that different life-cycle stages of the
malaria parasite, Plasmodium, share
antigens, thus allowing for the possibility of eliciting immunity to a parasite life-cycle stage that has not been experienced before. Using the Plasmodium chabaudi (AS strain) model of
malaria in mice, we investigated how isolated exposure to blood-stage
infection, bypassing a liver-stage
infection, yields significant protection to sporozoite challenge resulting in lower liver parasite burdens.
Antibodies are the main immune driver of this protection.
Antibodies induced by blood-stage
infection recognise
proteins on the surface of sporozoites and can impair sporozoite gliding motility in vitro, suggesting a possible function in vivo. Furthermore, mice lacking B cells and/or secreted
antibodies are not protected against a sporozoite challenge in mice that had a previous blood-stage
infection. Conversely, effector CD4+ and CD8+ T cells do not seem to play a role in protection from sporozoite challenge of mice previously exposed only to the blood stages of P. chabaudi. The protective response against pre-erythrocytic stages can be induced by
infections initiated by serially passaged blood-stage parasites as well as recently mosquito transmitted parasites and is effective against a different strain of P. chabaudi (CB strain), but not against another rodent
malaria species, P. yoelii. The possibility to induce protective cross-stage
antibodies advocates the need to consider both stage-specific and cross-stage immune responses to
malaria, as natural
infection elicits exposure to all life-cycle stages. Future investigation into these cross-stage
antibodies allows the opportunity for candidate
antigens to contribute to
malaria vaccine development.