IMMUNITY TO PLASMODIUM-BERGHEI-YOELII IN MICE .2. SPECIFIC AND NONSPECIFIC CELLULAR AND HUMORAL RESPONSES DURING COURSE OF INFECTION

Abstract

The kinetics of various specific and nonspecific immunologic responses were examined in BALB/c mice infected with 17X nonlethal P. berghei yoelii (a self-limiting infection). The sequence of events after infection was characterized by rapid sensitization of splenic T [thymus derived] cells to malaria antigen and polyclonal B [bone marrow derived] cell activation, followed by a period of depressed splenic proliferative responses in vitro to mitogens (PHA [phytohemagglutin] and LPS [lipopolysaccharide]) and malaria (specific) antigen. At the same time, suppressed primary in vitro splenic PFC [plaque forming cell] responses to trinitrophenyl-aminoethylcarbamylmethyl-Ficoll (TNP-F) were seen. This suppression was an active process requiring adherent cells. During this period, levels of antimalarial antibody also increased exponentially. As the infection was cleared, splenic malaria antigen-specific proliferative responses were again observed and splenic PFC and in vitro mitogen responses returned to preinfection levels after variable periods of time. Splenic proliferative responses to malaria antigen and antimalarial antibody responses remained persistently elevated. In addition, some responses were examined in mice infected with 17X lethal P. berghei yoelii (a fatal infection); in comparison to the early responses of mice infected with the nonlethal substrain, there was a decrease and delay in the development of a splenic T cell response to malaria antigen and a blunted antimalarial antibody response.