Abstract
B-1 B cells are a self-renewing population of B cells that differ from conventional B cells (B-2 cells) in that they are particularly predisposed to auto-antibody production. Although much is known about the signalling pathways that control B-1-cell growth and development, less is known about why these cells are prone to produce autoreactive antibodies. Here we show that B-1 cells, like germinal-centre B cells, can express recombinase-activating genes 1 and 2 (RAG1 and RAG2) and undergo secondary V(D)J recombination of immunoglobulin genes. In addition, B cells from autoimmune-prone NZB mice show high levels of RAG messenger RNA and recombination. We propose that secondary immunoglobulin-gene rearrangements outside organized lymphoid organs may contribute to the development of autoreactive antibodies.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Antigens, Nuclear*
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B-Lymphocytes / cytology*
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Cell Division
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DNA Helicases*
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DNA-Binding Proteins / genetics
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Gene Rearrangement, B-Lymphocyte*
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Genes, RAG-1
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Immunoglobulin Idiotypes / genetics
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Immunoglobulin J-Chains / genetics
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Immunoglobulin Variable Region / genetics
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Ku Autoantigen
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Mice
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Mice, Inbred Strains
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Nuclear Proteins / genetics
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Peritoneum / cytology
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Polymerase Chain Reaction
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Recombination, Genetic
Substances
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Antigens, Nuclear
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DNA-Binding Proteins
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Immunoglobulin Idiotypes
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Immunoglobulin J-Chains
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Immunoglobulin Variable Region
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Nuclear Proteins
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Rag2 protein, mouse
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V(D)J recombination activating protein 2
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DNA Helicases
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XRCC5 protein, human
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Xrcc6 protein, human
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Xrcc6 protein, mouse
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Ku Autoantigen