Journal
ISCIENCE
Volume 24, Issue 2, Pages -Publisher
CELL PRESS
DOI: 10.1016/j.isci.2021.102038
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Funding
- BBSRC [BB/M025292/1]
- National Council of Science and Technology, Mexico (CONACYT-Mexico)
- BBSRC [BB/S003800/1, BB/M025292/1] Funding Source: UKRI
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The study found that BCR signaling not only influences B cell selection and proliferation, but also can trigger cell apoptosis and suppress affinity maturation in the long term.
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 C gamma 1(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.
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