Abstract
T cell hybridomas require the immediate-early gene NGFI-B (nur77) for T cell receptor (TCR)-mediated apoptosis, a model for negative selection of self-reactive T cells. TCR-mediated death was examined in mice bearing an NGFI-B loss-of-function mutation, either by administration of antibodies to CD3 (anti-CD3) or in two well-characterized transgenic models expressing self-reactive TCRs. Both the extent and the rate of thymocyte death were unimpaired. Anti-CD3-induced death was normal in CD4+ peripheral T cells, in which death is mediated predominantly by the Fas signaling pathway. Thus, no unique requirement for NGFI-B is observed for thymic or peripheral T cell death.
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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Antibodies
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Apoptosis*
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CD3 Complex / immunology
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CD3 Complex / physiology
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Cells, Cultured
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Clonal Deletion
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Crosses, Genetic
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DNA-Binding Proteins / genetics
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DNA-Binding Proteins / physiology*
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Female
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Gene Targeting
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Hybridomas
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Male
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Mice
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Mice, Transgenic
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Nuclear Receptor Subfamily 4, Group A, Member 1
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Receptors, Antigen, T-Cell, alpha-beta / physiology*
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Receptors, Cytoplasmic and Nuclear
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Receptors, Steroid / genetics
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Receptors, Steroid / physiology*
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Stem Cells
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T-Lymphocyte Subsets / cytology
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T-Lymphocytes / cytology*
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T-Lymphocytes / immunology
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Thymus Gland / cytology
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Transcription Factors / genetics
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Transcription Factors / physiology*
Substances
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Antibodies
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CD3 Complex
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DNA-Binding Proteins
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Nr4a1 protein, mouse
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Nuclear Receptor Subfamily 4, Group A, Member 1
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Receptors, Antigen, T-Cell, alpha-beta
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Receptors, Cytoplasmic and Nuclear
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Receptors, Steroid
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Transcription Factors