One or another of these aspects has previously been observed in models of immunization or infection but rarely all four in one model.27–29,50–54 It is tempting to speculate that the reason for such variation is because TFR-mediated suppression may be primarily and most efficiently targeted toward the BDA-reactive spontaneous GC component, which, to various extent, co-exists within immunization- or infection-induced GCs. Here, TFRC is linked to infection.