Abstract
The interleukin-1 beta (IL-1 beta) converting enzyme (ICE) processes the inactive IL-1 beta precursor to the proinflammatory cytokine. Adherent monocytes from mice harboring a disrupted ICE gene (ICE-/-) did not export IL-1 beta or interleukin-1 alpha (IL-1 alpha) after stimulation with lipopolysaccharide. Export of tumor necrosis factor-alpha and interleukin-6 (IL-6) from these cells was also diminished. Thymocytes from ICE-/- mice were sensitive to apoptosis induced by dexamethasone or ionizing radiation, but were resistant to apoptosis induced by Fas antibody. Despite this defect in apoptosis, ICE-/- mice proceed normally through development.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Amino Acid Sequence
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Animals
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Antibodies, Monoclonal / immunology
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Antigens, Surface / immunology
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Apoptosis* / drug effects
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Apoptosis* / radiation effects
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Base Sequence
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Caspase 1
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Cells, Cultured
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Chimera
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Cysteine Endopeptidases / deficiency
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Cysteine Endopeptidases / metabolism*
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Cytokines / metabolism*
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Dexamethasone / pharmacology
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Female
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Interleukin-1 / metabolism
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Lipopolysaccharides / pharmacology
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Male
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Mice
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Mice, Inbred C57BL
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Molecular Sequence Data
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Monocytes / immunology*
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Nigericin / pharmacology
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T-Lymphocytes / cytology*
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fas Receptor
Substances
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Antibodies, Monoclonal
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Antigens, Surface
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Cytokines
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Interleukin-1
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Lipopolysaccharides
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fas Receptor
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Dexamethasone
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Cysteine Endopeptidases
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Caspase 1
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Nigericin