Abstract
Malaria infection dramatically induces two nonspecific perturbations in immune responsiveness, polyclonal B cell activation and immunosuppression. Polyclonal activation occurs early in infection and results in secretion of antibodies that lack antiplasmodial specificity. Immunosuppression occurs later in infection and is characterized by blunted humoral and cellular immune responses to heterologous (nonplasmodial) as well as plasmodial antigens. Previous studies have suggested that defects in macrophage function may be responsible for immunosuppression in malaria. In what way these cells might be altered in their immunoregulatory role during infection has not been clearly defined. One function of macrophages that is modified in malaria is the ability to secrete in vitro the monokine lymphocyte-activating factor (LAF). Adherent spleen cells obtained from mice early in Plasmodium berghei or P. yoelii infection secrete supernormal amounts of LAF. Adherent cells obtained later in infection show subnormal LAF-secreting activity and secrete an immunosuppressive substance. These modulations in macrophage function may be related to the quantity of parasite material ingested by these cells and might help explain the conversion of macrophages from a helper to a suppressor role in malaria.
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Selected References
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