Protection against a primary Babesia microti infection in mice, induced by the adoptive transfer of immune spleen cells, was abolished when the immune spleen cells were treated with mitomycin C prior to transfer. Since mitomycin C treatment prevents the replication of lymphocytes without affecting other cell functions, these results would suggest that the transferred cells required proliferation in the recipient mice before they could exert their protective effect, and this excludes the already differentiated antibody-forming cells (AFC's), macrophages and sensitised helper T cells. This was partly supported by the finding that Sephadex G-10 non-adherent immune cells, depleted of macrophages and AFC's, still conferred a strong protection after transfer. However, the Sephadex G-10 adherent cells, on a cell to cell basis, initially conferred a better protection against B. microti than did the non-adherent cells or unfractionated immune spleen cells. The possibility of the retention of an intermediate B memory cell type on the Sephadex G-10 columns and the suppression of antibody production are discussed in view of these results.