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B cells are generated from hematopoietic stem cells (HSCs) in the liver during the fetal life, and in the bone marrow in the adult. The differentiation pathway from HSC to mature B cell can be divided into several stages, based on the pheno- type and on functional properties that cells of the B lineage progressively acquire. Progenitor B (pro-B) cells can be iden- tified by cell surface expression of B220, CD43, and c-kit. Differential expression of heat-stable antigen (HSA) and of the maturation marker BP-1 discriminates four fractions of pro-B cells (fractions A, B, C, and C 9 (1)). At this stage of de- velopment, DNA rearrangement begins in the Ig H chain lo- cus. Most pro-B cells of fraction A carry Ig genes in germline configuration. D H φι J H rearrangements are found in almost all cells of fraction B. V H φι D H J H rearrangement occurs in frac- tions C and C 9 (2). Cells in fractions B to C 9 are also called pre-B I cells. As soon as m H chain proteins appear in the cy- toplasm and can be assembled into a functional precursor B cell receptor (pre-BCR), pre-B I cells develop into large pre-B II cells that are c-kit and CD43 negative (3). Successful rearrangement of the H chain and a correctly assembled pre- BCR associated with a functional signaling machinery allow pre-B II cells to proliferate. How is this proliferation con- trolled, what stimulates it, and what terminates it? When pro- liferation stops, pre-B II cells become smaller (so-called small pre-B II) and rearrangement starts again, this time in the L chain locus. Immature B cells subsequently express a com- plete IgM molecule on their surface. B cells leave the bone marrow at the transitional B cell stage and complete their final development into mature B cells in the periphery (4).

The Development of B Cells in the Bone Marrow Is Controlled by the Balance between Cell-Autonomous Mechanisms and Signals from the Microenvironment