In recent studies (1-3) it has been demonstrated that the passive transfer of imrnunocompetent allogeneic lymphoid cells to guinea pigs previously primed with 2,4-dinitrophenyl-ovalbumin (DNP-OVA) 1 results in the increased synthesis of anti-DNP and anti-OVA antibodies in the absence of further antigenic challenge, and markedly enhances anti-DNP responses to an appropriately timed challenge with DNP coupled to an unrelated carrier, bovine gamma globulin (BGG). This phenomenon has been termed the "allogeneic effect" and has several salient features. First, the phenomenon reflects and requires the development of a transient graftversus-host (GVtt) reaction in the lymphoid organs of the primed host (1). The existence of a concomitant host rejection reaction is not only not required, but appears to play little if any role (3). Secondly, the lymphoid cells of the host must be primed before the administration of allogeneic cells. Numerous attempts to demonstrate an enhanced primary response by the prior administration of allogeneic cells have failed, and, indeed, the primary response is usually suppressed under these circumstances (1-3a). Finally, the allogeneic effect has been shown to replace the requirement for carrier-specific helper T cells in the development of hapten-specific anamnestic antibody responses manifested by the primed lymphoid cells of the host (2).The studies presented in this and the accompanying paper (4) were undertaken in inbred mice to elucidate further the phenomenon of the allogeneic effect, in that, as a model, the mouse provides greater flexibility in manipulating cell populations and histocompatibility differences. In the experiments described here, we show that: (a) the general features of the allogeneic effect