CBA mice that recover from Plasmodium yoelii 17X infection are resistant to reinfection. T cells from these mice transfer immunity to nonimmune recipients. To analyze the nature and mode of action of these T cells, we transferred selected subsets into T cell-deprived recipients. Treatment of the T cells with anti-Ly-1 but not anti-Ly-2 serum and C abrogated their ability to transfer immunity. A mixture of anti-Ly-1 and anti-Ly-2 serum-treated cells (i.e., a population devoid of Ly-123 cells) transferred a level of immunity comparable to that of unselected T cells. Hence, the T cells mediating resistance to P. yoelii 17X were primarily of the Ly-1+23- phenotype. T cell-deprived mice reconstituted with these immune Ly-1 cells developed a) high levels of IgM and IgG antibodies, b) DTH responses to parasitized RBC, and c) enhanced blood monocyte responses. The addition of immune B cells to the Ly-1 population dramatically increased its ability to transfer immunity and induce antibody production. B cells from immune CBA/N mice had no such effect. Thus, the transfer of optimal protective immunity against malaria stems from an interaction between Ly-1 cells and a select B cell subset that CBA/N mice lack. This "selective synergy" is a protective mechanism against pathogens that has not been previously appreciated.