ALTERED CYTOKINE EXPORT AND APOPTOSIS IN MICE DEFICIENT IN INTERLEUKIN-1-BETA CONVERTING-ENZYME

被引:1469
作者
KUIDA, K
LIPPKE, JA
KU, G
HARDING, MW
LIVINGSTON, DJ
SU, MSS
FLAVELL, RA
机构
[1] VERTEX PHARMACEUT INC, CAMBRIDGE, MA 02139 USA
[2] YALE UNIV, SCH MED, HOWARD HUGHES MED INST, NEW HAVEN, CT 06510 USA
[3] YALE UNIV, SCH MED, IMMUNOBIOL SECT, NEW HAVEN, CT 06510 USA
关键词
D O I
10.1126/science.7535475
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
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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页码:2000 / 2003
页数:4
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