| First Author | Schiepers A | Year | 2024 |
| Journal | Immunity | Volume | 57 |
| Issue | 7 | Pages | 1618-1628.e4 |
| PubMed ID | 38838672 | Mgi Jnum | J:350982 |
| Mgi Id | MGI:7665170 | Doi | 10.1016/j.immuni.2024.05.009 |
| Citation | Schiepers A, et al. (2024) Opposing effects of pre-existing antibody and memory T cell help on the dynamics of recall germinal centers. Immunity 57(7):1618-1628.e4 |
| abstractText | Re-exposure to an antigen generates abundant antibody responses and drives the formation of secondary germinal centers (GCs). Recall GCs in mice consist almost entirely of naive B cells, whereas recall antibodies derive overwhelmingly from memory B cells. Here, we examine this division between cellular and serum compartments. After repeated immunization with the same antigen, tetramer analyses of recall GCs revealed a marked decrease in the ability of B cells in these structures to bind the antigen. Boosting with viral variant proteins restored antigen binding in recall GCs, as did genetic ablation of primary-derived antibody-secreting cells through conditional deletion of Prdm1, demonstrating suppression of GC recall responses by pre-existing antibodies. In hapten-carrier experiments in which B and T cell specificities were uncoupled, memory T cell help allowed B cells with undetectable antigen binding to access GCs. Thus, antibody-mediated feedback steers recall GC B cells away from previously targeted epitopes and enables specific targeting of variant epitopes, with implications for vaccination protocols. |
