Abstract
Tumor necrosis factor (TNF) mediates its biological effects by binding to two distinct but homologous receptor molecules. The type 1 receptor (TNF-R1) has been shown to be essential and sufficient for most cellular responses to soluble TNF. In contrast, only limited data exist concerning the role of the type 2 receptor (TNF-R2) in TNF responses, both in vitro and in vivo. Here, we demonstrate by the use of thymocytes from TNF-R-deficient mice that the TNF-R2-dependent enhancement of proliferation and secretion of granulocyte-macrophage colony-stimulating factor is in fact mediated by TNF-R2 on its own, independent of co-expression and/or stimulation of TNF-R1.
Publication types
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Comparative Study
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Antigens, CD / genetics
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Antigens, CD / metabolism
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Antigens, CD / physiology*
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Concanavalin A / pharmacology
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Granulocyte-Macrophage Colony-Stimulating Factor / metabolism
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Humans
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Lymphocyte Activation*
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Mice
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Mice, Knockout
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Receptors, Tumor Necrosis Factor / genetics
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Receptors, Tumor Necrosis Factor / metabolism
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Receptors, Tumor Necrosis Factor / physiology*
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Receptors, Tumor Necrosis Factor, Type I
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Receptors, Tumor Necrosis Factor, Type II
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Recombinant Proteins / pharmacology
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T-Lymphocytes / immunology*
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T-Lymphocytes / metabolism
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Thymus Gland / cytology
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Tumor Necrosis Factor-alpha / pharmacology*
Substances
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Antigens, CD
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Receptors, Tumor Necrosis Factor
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Receptors, Tumor Necrosis Factor, Type I
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Receptors, Tumor Necrosis Factor, Type II
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Recombinant Proteins
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Tumor Necrosis Factor-alpha
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Concanavalin A
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Granulocyte-Macrophage Colony-Stimulating Factor