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. 2021 Mar 6;14:40. doi: 10.1186/s13045-021-01049-7

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© The Author(s) 2021

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 2 — BCR in B cell development. In the bone marrow, progenitor B (pro-B) cells undergo the rearrangement and development of immunoglobulin heavy-chain variable (V), diversity (D), and joining (J) gene segments to form the pre-BCR. The pre-BCR is an immature form of the BCR providing signals for survival, proliferation, and cellular differentiation. After light-chain gene rearrangement occurs, immature B cells express BCR, leave the bone marrow, and mature in the periphery. Mature B cells undergo somatic hypermutation (SHM) driven by the expression of activation-induced cytidine deaminase (AID) in the germinal center (GC) to complete BCR affinity maturation and antibody diversification. The genotoxic stress induced by SHM may lead to the apoptosis of these B cells. However, the continuous BCR signaling could provide pro-survival signals for these B cells, thereby preventing them from apoptosis. Therefore, B cells deficient in Bruton tyrosine kinase tend to undergo apoptosis during the development. The B cells that have completed affinity maturation and antibody diversification then undergo class-switch recombination (CSR), after which they develop into memory B cells with high-affinity BCRs or plasma cells secreting antibodies. DZ, dark zone; LZ, light zone; FDC, follicular dendritic cell; Tfh cell, T follicular helper cell