Abstract
Survival and phenotype of normal and malignant B lymphocytes are critically dependent on constitutive signals by the B cell receptor (BCR) for antigen. In addition, either antigen ligation of the BCR or various mitogenic stimuli result in B cell activation and induction of activation-induced deaminase (AID). AID activity can in turn mediate somatic hypermutation (SHM) of immunoglobulin (Ig) V regions and also deeply remodel the Ig heavy chain locus through class switch recombination (CSR) or locus suicide recombination (LSR). In addition to changes linked to affinity for antigen, modifying the class/isotype (i.e. the structure and function) of the BCR or suddenly deleting BCR expression also modulates the fate of antigen-experienced B cells.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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AICDA (Activation-Induced Cytidine Deaminase)
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Apoptosis
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B-Lymphocytes / immunology
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B-Lymphocytes / metabolism*
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Cell Differentiation*
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Cytidine Deaminase / metabolism
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Cytidine Deaminase / physiology*
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Gene Conversion
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Humans
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Immunoglobulin Class Switching / genetics
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Immunoglobulin Heavy Chains / genetics
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Immunoglobulin Heavy Chains / metabolism
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Immunoglobulin Variable Region / genetics
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Immunoglobulins / genetics*
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Immunoglobulins / immunology
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Immunoglobulins / metabolism*
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Mutation
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Receptors, Antigen, B-Cell / genetics*
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Receptors, Antigen, B-Cell / immunology
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Receptors, Antigen, B-Cell / metabolism*
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Signal Transduction
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Somatic Hypermutation, Immunoglobulin
Substances
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Immunoglobulin Heavy Chains
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Immunoglobulin Variable Region
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Immunoglobulins
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Receptors, Antigen, B-Cell
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AICDA (Activation-Induced Cytidine Deaminase)
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Cytidine Deaminase