Journal
IMMUNOLOGIC RESEARCH
Volume 27, Issue 1, Pages 31-51Publisher
HUMANA PRESS INC
DOI: 10.1385/IR:27:1:31
Keywords
B-cell antigen receptor; B-1 cells; B-2 cells; B cell development; D-type cyclins; cyclin-dependent kinases; cell cycle; retinoblastoma gene product; immature B lymphocytes
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Funding
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R21AI049994, R01AI029690, R01AI049994, R21AI029690, R56AI029690] Funding Source: NIH RePORTER
- NIAID NIH HHS [AI29690, AI49994] Funding Source: Medline
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An effective humoral response requires that a given B lymphocyte population express a repertoire of receptors capable of recognizing a distinct array of antigens, while at the same time disregarding self-antigens. Mature B cells interacting with antigen via their B cell antigen receptors (BCRs) enter G, phase of the cell cycle and, depending on the strength of the signal, can commit to S phase entry. Input from co-receptors, which may function to either enhance or inhibit BCR signals, also influence the decision to proliferate. We review herein recent advances in the biochemistry of G(1)-cyclin holoenzymes that function to integrate BCR-coupled signaling pathways to the phosphorylation (and inactivation) of the retinoblastoma gene product (pRb) in splenic B lymphocytes (B-2 cells). We also highlight differences in the control of G(1)-to-S phase progression between B-2 cells and peritonea] CD5(+) B cells (B-1 cells).
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