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

被引：1476

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

来源：

SCIENCE | 1995年 / 267卷 / 5206期

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.

引用

页码：2000 / 2003

页数：4

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