Abstract
The bcl-2 proto-oncogene can prevent the death of many cell types. Mice were generated that were chimeric for the homozygous inactivation of bcl-2. Lymphocytes without Bcl-2 differentiated into phenotypically mature cells. However, in vitro, the mature T cells that lacked Bcl-2 had shorter life-spans and increased sensitivity to glucocorticoids and gamma-irradiation. In contrast, stimulation of CD3 inhibited the death of these cells. T and B cells with no Bcl-2 disappeared from the bone marrow, thymus, and periphery by 4 weeks of age. Thus, Bcl-2 was dispensable for lymphocyte maturation, but was required for a stable immune system after birth.
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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Apoptosis
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B-Lymphocytes / cytology
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B-Lymphocytes / immunology*
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Base Sequence
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Bone Marrow / immunology
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Bone Marrow Cells
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CD3 Complex / immunology
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Cell Line
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Chimera
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Homozygote
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Humans
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Lymphoid Tissue / cytology
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Lymphoid Tissue / immunology
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Mice
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Mice, Inbred C57BL
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Molecular Sequence Data
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Proto-Oncogene Mas
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Proto-Oncogene Proteins / genetics
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Proto-Oncogene Proteins / physiology*
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Proto-Oncogene Proteins c-bcl-2
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Proto-Oncogenes
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Receptors, Antigen, T-Cell / immunology
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T-Lymphocytes / cytology
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T-Lymphocytes / immunology*
Substances
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CD3 Complex
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MAS1 protein, human
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Proto-Oncogene Mas
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Proto-Oncogene Proteins
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Proto-Oncogene Proteins c-bcl-2
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Receptors, Antigen, T-Cell