Cellular Signaling Events in B Lymphocytes

  • Margaret M. Harnett
Part of the Blood Cell Biochemistry book series (BLBI, volume 7)


The B lymphocyte is the principal cellular mediator of the specific humoral immune response to infection. B cells arise from pluripotent stem cells in the bone marrow via a number of well-defined precursor B-cell phenotypes in a complex process that integrates signals generated by a number of immunoregulatory receptors on several cell types, often in specialized environments (Cushley and Harnett, 1993). Once B cells emerge into the periphery, selection of the appropriate clones by antigen can lead to (1) cellular anergy and/ or apoptosis of immature B cells, (2) activation and proliferation of mature B cells, or (3) rescue of germinal center cells from cell suicide followed by differentiation into antibody-secreting plasma cells or memory B cells (reviewed by Cushley and Harnett, 1993). The mechanism by which the antigen receptors (mlg) on B cells can elicit these different biological responses in a maturation-state-dependent manner is one of the central problems in B-cell differentiation yet to be resolved. However, it is clear that many of the signaling events involved in these biological responses are regulated by both cytokines (reviewed by O’Garra et al., 1988) and membrane-associated ligands on helper T cells (reviewed by Clark and Lane, 1991). Characterization of the B-cell receptors that can process these signals has generated a unifying model of (interacting) coreceptor complexes (e.g., CD19/CD21, CD22, CD38, and CD40) and cytokine receptors (e.g., IL-4R) that can modulate mIg-mediated B-cell activation (reviewed by Harnett, 1994).


Tyrosine Phosphorylation Protein Tyrosine Kinase Cytoplasmic Tail Antigen Receptor Cell Antigen Receptor 
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Copyright information

© Springer Science+Business Media New York 1996

Authors and Affiliations

  • Margaret M. Harnett
    • 1
  1. 1.Division of Biochemistry and Molecular BiologyUniversity of GlasgowGlasgowUK

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