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Part of the book series: Current Topics in Microbiology and Immunology ((CT MICROBIOLOGY,volume 245/1))

Abstract

The development of B lymphocytes (Fig. 1) from committed precursor cells to antibody-producing plasma cells proceeds through multiple stages defined by the expression of distinct sets of lineage-specific genes (Rolink and Melchers 1996). The early, antigen-independent stages of B-cell differentiation were largely defined by the status of the cell’s immunoglobulin (Ig) genes. In the scheme advanced by Rolink and Melchers (1996), pro-B cells are defined as cells that are committed to the B-cell lineage, but have not yet undergone any Ig gene rearrangements. At the early pre-B cell stage (pre-BI), cells activate their Ig gene recombination machinery including the RAG-1 and RAG-2 genes and commence rearrangements at Ig heavy-chain loci. Heavy-chain polypeptides associate with surrogate light chains encoded by the VpreB and λ5 genes and accessory polypeptides encoded by the mb-1 (Igα/CD79a) and B29 (Igβ/CD79b) genes to assemble the pre-B cell receptor (pre-BCR) on the plasma membrane. Following the productive rearrangement of κ or λ, light chain gene loci, mature membrane-bound Ig (mIg) appears on the plasma membrane of immature B cells as the B-cell receptor (BCR) for antigen. Encounter of specific antigen by a B cell results in intracellular signaling events that can promote further differentiation, including Ig heavy-chain class switch recombination, somatic hypermutation of Ig variable-region genes, and receptor editing. Ultimately, B cells can terminally differentiate to become plasma cells, which do not express Ig on the cell surface and secrete large quantities of antibody.

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Hagman, J., Wheat, W., Fitzsimmons, D., Hodsdon, W., Negri, J., Dizon, F. (2000). Pax-5/BSAP: Regulator of Specific Gene Expression and Differentiation in B Lymphocytes. In: Justement, L.B., Siminovitch, K.A. (eds) Signal Transduction and the Coordination of B Lymphocyte Development and Function I. Current Topics in Microbiology and Immunology, vol 245/1. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-57066-7_5

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