Re-exposure to an antigen generates serum antibody responses that greatly exceed in magnitude those elicited by primary antigen encounter, while simultaneously driving the formation of recall germinal centers (GCs). Although recall GCs in mice are composed almost entirely of naïve B cells, recall antibody titers derive overwhelmingly from memory B cells, suggesting a division between cellular and serum compartments. Here, we show that this schism is at least partly explained by a marked decrease in the ability of recall GC B cells to detectably bind antigen. Variant priming and plasmablast ablation experiments show that this decrease is largely due to suppression by pre-existing antibody, whereas hapten-carrier experiments reveal a role for memory T cell help in allowing B cells with undetectable antigen binding to access GCs. We propose a model in which antibody-mediated feedback steers recall GC B cells away from previously targeted epitopes, thus enabling specific targeting of variant epitopes.