Mice immunized with 2,4-dinitrophenyl-bovine serum albumin (DNP-BSA) show a greater anti-ovalbumin (OVA) antibody response to subsequent immunization with DNP-OVA than do mice initially immunized with BSA alone. In order to determine the mechanism of this DNP-specific augmentation of anti-OVA antibody response to DNP-OVA, we performed cell and serum transfer experiments. Irradiated recipient mice received spleen cells from donor mice which had been primed with OVA and subsequently treated with heterologous anti-mouse lymphocyte serum; these cells served as precursors of anti-OVA antibody-forming cells. Such recipients made greatly augmented anti-OVA responses to DNP-OVA if they also received serum from mice primed with DNP-keyhole limpet hemocyanin (KLH). Spleen cells from DNP-KLH primed donors transferred little or no augmentation of this response, and such activity as they possessed appears to be due to the anti-DNP antibody they secrete. Anti-DNP antibody purified by elution from a solid immunoadsorbent possessed all the augmenting activity of anti-DNP-KLH serum. These experiments provide no evidence for functionally active, thymus-derived, hapten-specific “helper” cells. The implications of this result are discussed.