Enhanced BCR signaling inflicts early plasmablast and germinal center B cell death
Juan Carlos Yam‐Puc, Lingling Zhang, Raul A. Maqueda‐Alfaro, Laura Garcia‐Ibanez, Yang Zhang, Jessica L. Davies, Yotis A. Senis, Michael Snaith, Kai‐Michael Toellner
Abstract
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.