Abstract
B cell homeostasis is maintained by a balance between the continual generation of new cells and their elimination. Here we show proapoptotic BCL-2 family members BAX and BAK are essential for regulating the number of B cells at both immature and mature developmental stages. BAX and BAK are critical mediators of B cell death induced by multiple stimuli. In addition, BAX- and BAK-deficient B cells display defective cell cycle progression to B cell receptor crosslinking and lipopolysaccharide, but not to CpG-DNA. Furthermore, inducible deletion of Bax and Bak in adult mice results in the development of severe autoimmune disease.
Publication types
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Comparative Study
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Apoptosis / immunology*
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Apoptosis Regulatory Proteins / genetics
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Apoptosis Regulatory Proteins / immunology
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Autoimmune Diseases / immunology*
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B-Lymphocytes / immunology*
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Bcl-2-Like Protein 11
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Flow Cytometry
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Fluoresceins
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Immunohistochemistry
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Membrane Proteins / genetics
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Membrane Proteins / immunology
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Mice
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Mice, Knockout
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Proto-Oncogene Proteins / genetics
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Proto-Oncogene Proteins / immunology
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Succinimides
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bcl-2 Homologous Antagonist-Killer Protein / genetics
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bcl-2 Homologous Antagonist-Killer Protein / immunology*
Substances
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5-(6)-carboxyfluorescein diacetate succinimidyl ester
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Apoptosis Regulatory Proteins
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Bak1 protein, mouse
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Bcl-2-Like Protein 11
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Bcl2l11 protein, mouse
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Fluoresceins
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Membrane Proteins
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Proto-Oncogene Proteins
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Succinimides
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bcl-2 Homologous Antagonist-Killer Protein