Abstract

Our data indicate that, in addition to canonical T_FR cells, there exists a second population of Foxp3 GC T cells that arises immediately before GC contraction, through the up-regulation of Foxp3 and limited acquisition of T_reg-like features by T_FH cells. Functional experiments support a model in which the contraction, and eventual shutdown, of late-stage GCs is promoted by acquisition of Foxp3 by this T_FH cell population. These findings raise the possibility that GC shutdown is an active process rather than simply a result of the progressive consumption of antigen by GC B cells. Manipulating this process may provide an avenue toward extending GC lifetime, potentially contributing to the induction of highly mutated antibodies by vaccination.