T-cell activation in murine malaria.

Abstract

THE immune response of rodents to malaria is thymus dependent. Plasmodium berghei infections are more severe in neonatally thymectomised rats than in intact controls1, whereas P. yoelii (P. berghei yoelii) infections which are self-resolving in normal CBA mice prove fatal in T-cell deprived CBA mice (Jayawardena et al., unpublished) or congenitally athymic nude mice2. Malarial infections are also known to depress immune responses to certain antigens. In the mouse, they reduce the antibody3 and splenic plaque forming cell4 response to sheep red blood cells (SRBCs), render animals more susceptible to lymphomagenic viruses5, and severe long term infections prolong xenogeneic skin graft survival time6. It has been suggested that such impaired immune reactivity reflects defective lymphocyte or macrophage function, but there has been no unequivocal evidence in support of these possibilities.