IMMUNITY TO ERYTHROCYTIC STAGES OF MALARIAL PARASITES

In those individuals who live in endemic areas, immunity to malaria is slow to develop and stage-specific. The nature and antigenic specific ity of this response, which may involve components of both cell-mediat ed and humoral immunity, is not well understood. Rodent models provide useful systems to explore the spectrum of host responses that may con tribute to resolution of erythrocytic-stage infection or possibly to p athogenesis. Moreover, these models allow identification of plasmodial molecules that can induce different types of host responses. Two diff erent mouse model systems, Plasmodium yoelii yoelii and P. chabaudi ad ami are presented. These have been selected because resolution of infe ction by P. yoelii yoelii has been shown to require B cell-dependent m echanisms, while control of acute P. chabaudi adami infection can be a chieved by T cell-dependent mechanisms. A monoclonal antibody that pro vides passive protection to P. yoelii challenge infection has been sho wn to recognize the cysteine-rich, carboxyl-terminal region of the mer ozoite surface protein-1. This region, obtained in an appropriate conf iguration from recombinant Escherichia coli, can induce significant pr otective immune responses in naive mice. In contrast, cell-mediated im mune mechanisms make a major contribution to resolution of asexual-sta ge P. chabaudi adami infection. An empirical approach using continuous flow electrophoresis has identified several low molecular weight plas modial proteins that can induce partial protective responses in suscep tible hosts. These observations are briefly discussed with respect to human malaria.