Protection against infection with Babesia microti in mice was passively transferred with either serum or cells. Immune spleen cells were more effective than were immune mesenteric lymph node (MLN) cells in reducing parasitaemias in recipient mice, and the level of protection correlated with the donor to recipient ratio rather than with the number of cells transferred. Protection against primary infection in recipient mice was adoptively transferred by nylon wool adherent, B cell enriched subpopulations of spleen cells. In contrast, higher peak parasitaemias were apparent in mice which received nylon wool non-adherent, T enriched spleen cells in comparison with the control mice. However, if the recipient mice were reinfected, control of this second infection was greatest in the recipients of the T enriched cell subpopulation. Treatment of the protective nylon wool adherent, B cell subpopulation with anti-theta serum and complement abolished both the protective effect and the anamnestic antibody response in the recipient mice. This suggested that primed T cells controlled the expression of the protective antibody response by primed B cells.