Altered Cytokine Export and Apoptosis in Mice Deficient in Interleukin-1β Converting Enzyme
Keisuke Kuida(Howard Hughes Medical Institute), Judith A. Lippke(Vertex Pharmaceuticals (United States)), George Ku(Vertex Pharmaceuticals (United States)), Matthew W. Harding(Vertex Pharmaceuticals (United States)), David J. Livingston(Howard Hughes Medical Institute), Michael Su(Vertex Pharmaceuticals (United States)), Richard A. Flavell(Howard Hughes Medical Institute)
Cited by 1,626
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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