Abstract
At the end of the T cell response, the majority of the activated T cells die. We activated Vbeta8(+) T cells with staphylococcal enterotoxin B (SEB) in vivo and monitored the expansion and deletion of Vbeta8(+) T cells. We found that, in response to SEB, activated T cells died in vivo in the absence of Fas or TNF-R signaling but not when they overexpressed human Bcl-2. We also found that Vbeta8(+) T cells from Bim-deficient mice are resistant to SEB-induced deletion. While Bim levels did not change, endogenous Bcl-2 levels within Vbeta8(+) T cells decrease following SEB injection. Thus, the death of superantigen-stimulated T cells in vivo is mediated by Bim and may be modulated by a decrease in Bcl-2.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, Non-P.H.S.
MeSH terms
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Animals
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Apoptosis Regulatory Proteins
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Apoptosis*
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Bcl-2-Like Protein 11
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Carrier Proteins / physiology*
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Cell Line
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Down-Regulation
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Enterotoxins / pharmacology
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Female
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Flow Cytometry
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Lymphocyte Activation*
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Membrane Proteins*
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Mice
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Mice, Inbred C57BL
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Proto-Oncogene Proteins c-bcl-2 / metabolism
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Proto-Oncogene Proteins*
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Receptors, Antigen, T-Cell, alpha-beta*
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Receptors, Tumor Necrosis Factor / physiology
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Superantigens / pharmacology
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T-Lymphocytes / physiology*
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fas Receptor / pharmacology
Substances
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Apoptosis Regulatory Proteins
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BCL2L11 protein, human
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Bcl-2-Like Protein 11
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Bcl2l11 protein, mouse
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Carrier Proteins
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Enterotoxins
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Membrane Proteins
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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, alpha-beta
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Receptors, Tumor Necrosis Factor
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Superantigens
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fas Receptor
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enterotoxin B, staphylococcal