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      Altered cytokine export and apoptosis in mice deficient in interleukin-1 beta converting enzyme.

      Science (New York, N.Y.)
      Amino Acid Sequence, Animals, Antibodies, Monoclonal, immunology, Antigens, CD95, Antigens, Surface, Apoptosis, drug effects, radiation effects, Base Sequence, Caspase 1, Cells, Cultured, Chimera, Cysteine Endopeptidases, deficiency, metabolism, Cytokines, Dexamethasone, pharmacology, Female, Interleukin-1, Lipopolysaccharides, Male, Mice, Mice, Inbred C57BL, Molecular Sequence Data, Monocytes, Nigericin, T-Lymphocytes, cytology

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          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.

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