ABSTRACTThe 19-kDa carboxyl-terminal fragment of the merozoite surface protein-1 (MSP-119) has been shown to regulate antibody (Ab)-mediated protective immunity to blood-stage malaria infection. But the serological memory to this antigen tends to be short-lived, and little is known of the mechanisms that regulate the formation of B cell memory to MSP-119antigen. We studied the formation of B cell memory response after immunization with the recombinant 19-kDaPlasmodium falciparummerozoite surface protein 1 (PfMSP-119). Immunization with PfMSP-119resulted in delayed increase in germinal center (GC) B cell numbers. This poor GC reaction correlated with short-lived PfMSP-119-specific antibodies in serum and the short life of PfMSP-119-specific plasma cells and memory B cells (MBCs) in spleen and bone marrow. PfMSP-119-specific MBCs were capable of producing antigen (Ag)-specific Ab-secreting cell (ASC) responses that were short-lived following challenge immunization of the immune mice with antigen or transgenicPlasmodium bergheiparasite expressing PfMSP-119in place of nativeP. bergheiMSP-119at 8 weeks after the last immunization or following adoptive transfer into naive hosts. However, no protection was achieved in PfMSP-119immune mice or recipient mice with PfMSP-119-specific MBCs following challenge with transgenicP. berghei. Our findings suggest that PfMSP-119-specific IgG production by short-lived plasma cells combined with the poor ability of the PfMSP-119-induced MBCs to maintain the anamnestic IgG responses failed to contribute to protection against infection.
Long-Lived Antibody and B Cell Memory Responses to the Human Malaria Parasites, Plasmodium falciparum and Plasmodium vivax
