Jerne (1) has proposed that the immune system functions as an interacting network of inducible elements that normally exist in a steady state. In this network, the immune response is regulated by idiotype-anti-idiotype interactions. Antigen administration stimulates some elements of the network, and the subsequent alterations to restore the perturbed steady-state condition represent the cellular and molecular reactions that occur during the immune response.In many experimental systems that examine idiotype-anti-idiotype interactions, the anti-idiotypic antibodies have been induced in species other than the one in which the idiotype was produced (2-6). Induction of isologous anti-idiotypic antibodies has also been achieved (4-12). Spontaneous, autologous anti-idiotypic-antibody and (or) anti-receptor-antibody production during the course of an immune response has been described for haptens (13-16), sheep erythrocytes (SRBC) 1 (i 5, 16), and alloantigens (16)(17)(18)(19). In addition, the decrease in binding affinity of anti-tobacco mosaic virus antibodies has been attributed to the appearance, during the course of the immune response, of lymphocytes bearing auto-anti-idiotypic receptors (20).Although cyclic changes in serum-antibody levels and affinity have been observed during the immune response to many antigens, they have generally been attributed to variations in the degree of masking, by serum antibody, of antigenic determinants on persisting antigen (21,22). Nevertheless, a rapid decrease in affinity of individual plaque-forming cells (PFC) (23) or serum antibody (20, 24) cannot be convincingly explained in this manner. Urbain (25) has suggested that an auto-anti-idiotypic