| First Author | Yam-Puc JC | Year | 2021 |
| Journal | iScience | Volume | 24 |
| Issue | 2 | Pages | 102038 |
| PubMed ID | 33532715 | Mgi Jnum | J:308563 |
| Mgi Id | MGI:6717900 | Doi | 10.1016/j.isci.2021.102038 |
| Citation | Yam-Puc JC, et al. (2021) Enhanced BCR signaling inflicts early plasmablast and germinal center B cell death. iScience 24(2):102038 |
| abstractText | It is still not clear how B cell receptor (BCR) signaling intensity affects plasma cell (PC) and germinal center (GC) B cell differentiation. We generated Cgamma1 (Cre/wt) Ptpn6 (fl/fl) mice where SHP-1, a negative regulator of BCR signaling, is deleted rapidly after B cell activation. Although immunization with T-dependent antigens increased BCR signaling, it led to PC reduction and increased apoptosis. Dependent on the antigen, the early GC B cell response was equally reduced and apoptosis increased. At the same time, a higher proportion of GC B cells expressed cMYC, suggesting GC B cell-Tfh cell interactions may be increased. GC B cell numbers returned to normal at later stages, whereas affinity maturation was suppressed in the long term. This confirms that BCR signaling not only directs affinity-dependent B cell selection but also, without adequate further stimulation, can inflict cell death, which may be important for the maintenance of B cell tolerance. |
