Abstract
Encounters with antigen can stimulate T cells to become activated and proliferate, become nonresponsive to antigen, or to die. T cell death was shown to be a physiological response to interleukin-2-stimulated cell cycling and T cell receptor reengagement at high antigen doses. This feedback regulatory mechanism attenuates the immune response by deleting a portion of newly dividing, antigen-reactive T cells. This mechanism deleted autoreactive T cells and abrogated the clinical and pathological signs of autoimmune encephalomyelitis in mice after repetitive administration of myelin basic protein.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Antigens / immunology*
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Apoptosis
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CD4-Positive T-Lymphocytes / immunology*
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Cell Division
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Cells, Cultured
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Cytochrome c Group / immunology
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Dose-Response Relationship, Immunologic
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Encephalomyelitis, Autoimmune, Experimental / immunology*
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Encephalomyelitis, Autoimmune, Experimental / pathology
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Encephalomyelitis, Autoimmune, Experimental / therapy
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Immune Tolerance*
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Immunotherapy
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Interleukin-2 / immunology
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Interleukin-2 / pharmacology
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Lymphocyte Activation
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Mice
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Mice, Transgenic
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Myelin Basic Protein / immunology
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Myelin Sheath / immunology
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Myelin Sheath / pathology
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Spinal Cord / pathology
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T-Lymphocytes / immunology*
Substances
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Antigens
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Cytochrome c Group
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Interleukin-2
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Myelin Basic Protein