Cell cycle control mechanisms in B-1 and B-2 lymphoid subsets.
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(1) 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 peritoneal CD5+ B cells (B-1 cells).
Piatelli
Michael  J
M
Departments of Biology, Boston College, Chestnut Hill, MA 02467, USA.
Tanguay
Debra
D
Rothstein
Thomas  L
T
Chiles
Thomas  C
T
D000818:Animals; D016175:B-Lymphocyte Subsets / Q000166:cytology / Q000276:immunology*; D001402:B-Lymphocytes / Q000166:cytology / Q000276:immunology*; D002453:Cell Cycle / Q000276:immunology*; D002454:Cell Differentiation / Q000276:immunology; D018844:Cyclin-Dependent Kinases / Q000276:immunology; D016213:Cyclins / Q000276:immunology; D008213:Lymphocyte Activation / Q000276:immunology; D051379:Mice; D011947:Receptors, Antigen, B-Cell / Q000276:immunology*; D016160:Retinoblastoma Protein
D016213:Cyclins; D011947:Receptors, Antigen, B-Cell; D016160:Retinoblastoma Protein; D018844:Cyclin-Dependent Kinases