Carrier-induced epitopic suppression is initiated through clonal dominance.

Injection of mice with an immunogenic dose of carrier followed by immunization with hapten-carrier conjugate selectively suppresses anti-hapten antibody response. Previous studies have proposed that this epitopic suppression is related to the induction of carrier-specific Ts cells which in turn could inhibit selectively anti-hapten response. In the present study, we propose that the epitopic suppression is in fact due to clonal dominance. Immunization with a carrier such as tetanus toxoid induces a clonal expansion of carrier-specific B cells, thus decreasing the probability of hapten-specific B cells to react with the Ag. Increasing the density of the TNP-hapten on the conjugate has totally prevented the induction of the epitopic suppression. Moreover, using low hapten-carrier concentrations to challenge carrier-primed mice has enhanced the induction of the suppression. Finally, priming hapten-specific B cells before carrier/hapten-carrier immunization has also abrogated the suppression. The results of these experiments support the view that epitopic suppression is induced through the expansion of the clones specific for the carrier epitopes and resulted from intra-molecular antigenic competition between hapten and carrier epitopes. Based on these findings a regulatory role is proposed for B cells, where through their capacity to process and present antigen, they would exercise a strong influence on the selection of immune responses.