Abstract
B cells can revise their antigen receptors outside the confines of the bone marrow by secondary Ig gene rearrangements. Although the initial motivation to perform these revisions might be to silence a self-reactive specificity, those B cells that reinitiate the recombination process can perform a series of "leaping" rearrangements and inadvertently shift their receptor specificity towards autoimmunity. Heavy-chain receptor revision, coupled with other atypical rearrangements, might contribute to autoantibody production in systemic lupus erythematosus.
Publication types
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Research Support, U.S. Gov't, P.H.S.
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Review
MeSH terms
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Animals
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Autoimmunity / genetics
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Autoimmunity / immunology*
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DNA-Binding Proteins / genetics
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DNA-Binding Proteins / immunology
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Gene Rearrangement, B-Lymphocyte, Heavy Chain*
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Genes, Immunoglobulin
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Homeodomain Proteins / genetics
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Homeodomain Proteins / immunology
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Humans
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Immunoglobulin Heavy Chains / genetics*
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Immunoglobulin Heavy Chains / immunology
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Nuclear Proteins
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Receptors, Antigen, B-Cell / genetics
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Receptors, Antigen, B-Cell / immunology
Substances
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DNA-Binding Proteins
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Homeodomain Proteins
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Immunoglobulin Heavy Chains
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Nuclear Proteins
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RAG2 protein, human
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Receptors, Antigen, B-Cell
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V(D)J recombination activating protein 2
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RAG-1 protein