Abstract
The immune system normally avoids producing antibodies that react with autologous ("self") antigens by censoring self-reactive T and B cells. Unlike the T cell repertoire, antibody diversity is generated within the B cell repertoire in two phases; the first occurs by gene rearrangement in primary lymphoid organs, and the second phase involves antigen-driven hypermutation in peripheral lymphoid organs. The possibility that distinct cellular mechanisms may impose self tolerance at these two different phases of B cell diversification may explain recent findings in transgenic mouse models, in which self-reactive B cells appear to be silenced both by functional inactivation and by physical elimination.
Publication types
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Comparative Study
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Antibody Diversity / immunology
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Autoantibodies / biosynthesis
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Autoantibodies / immunology
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Autoantigens / immunology
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B-Lymphocytes / immunology*
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Binding Sites, Antibody
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Cell Survival
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Down-Regulation
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Gene Rearrangement, B-Lymphocyte
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H-2 Antigens / immunology
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Immune Tolerance*
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Mice
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Mice, Transgenic
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Muramidase / immunology
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Receptors, Antigen, B-Cell / genetics
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Receptors, Antigen, B-Cell / immunology
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Receptors, Antigen, T-Cell / genetics
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Receptors, Antigen, T-Cell / immunology
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T-Lymphocytes / immunology
Substances
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Autoantibodies
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Autoantigens
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H-2 Antigens
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Receptors, Antigen, B-Cell
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Receptors, Antigen, T-Cell
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Muramidase