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

Authors:
Kuida K, Lippke JA, Ku G, Harding MW, Livingston DJ, Su MS, Flavell RA
Affiliation:
Journal:
Science (New York, N.Y.)

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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