ABSTRACT
Plasmodium berghei infection gives rise to a fatal fulminating parasitaemia in mice. Resistance to the infection can be achieved if the mice are allowed to recover from the blood-induced infection by administration of chloroquine. In CBA/Caj, one cycle and in Balb/c mice, at least, two cycles of infection, alternating with drug-cure were necessary for the establishment of immunity. No parasitaemia was seen following further challenges after the third infection. Adoptive transfer of spleen cells from the immune mice showed that immunity could be transferred by 50 to 70 x 10(6) cells. On challenge the recipients develop high parasitaemia which was cleared in less than 5 weeks. Recipient mice given low number of spleen cells did not survive. The transfer of immune spleen cells depleted of either T or B lymphocytes abrogated the protective effect. Comparatively T lymphocytes were less effective in transferring protection than B lymphocytes. The study suggests that both humoral and cell-mediated effector mechanisms are needed for the maintenance of immunity in drug-cured immune mice.