We also observed substantial increases in the bulk serological affinity of influenza-specific antibodies in most of the FOXP3-deficient organoids and to a lesser extent in GZMB KOs; this is reminiscent of the increased affinity for self-specific antibodies in AIRE-deficient individuals53,54 and indicates that disrupting T cell tolerance allows the emergence of higher-affinity antibodies. Here, FOXP3 is linked to influenza.