ABSTRACT
The 19-kDa carboxyl-terminal fragment of the merozoite surface protein-1 (MSP-1(19)) 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-1(19) antigen. We studied the formation of B cell memory response after immunization with the recombinant 19-kDa Plasmodium falciparum merozoite surface protein 1 (PfMSP-1(19)). Immunization with PfMSP-1(19) resulted in delayed increase in germinal center (GC) B cell numbers. This poor GC reaction correlated with short-lived PfMSP-1(19)-specific antibodies in serum and the short life of PfMSP-1(19)-specific plasma cells and memory B cells (MBCs) in spleen and bone marrow. PfMSP-1(19)-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 transgenic Plasmodium berghei parasite expressing PfMSP-1(19) in place of native P. berghei MSP-1(19) at 8 weeks after the last immunization or following adoptive transfer into naive hosts. However, no protection was achieved in PfMSP-1(19) immune mice or recipient mice with PfMSP-1(19)-specific MBCs following challenge with transgenic P. berghei. Our findings suggest that PfMSP-1(19)-specific IgG production by short-lived plasma cells combined with the poor ability of the PfMSP-1(19)-induced MBCs to maintain the anamnestic IgG responses failed to contribute to protection against infection.
