ALTERED CYTOKINE EXPORT AND APOPTOSIS IN MICE DEFICIENT IN INTERLEUKIN-1-BETA CONVERTING-ENZYME
ALTERED CYTOKINE EXPORT AND APOPTOSIS IN MICE DEFICIENT IN INTERLEUKIN-1-BETA CONVERTING-ENZYME
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DOI：
10.1126/science.7535475
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发表时间：
1995-03-31
期刊：
影响因子：
56.9
通讯作者：
FLAVELL, RA
中科院分区：
文献类型：
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作者：
KUIDA, K;LIPPKE, JA;FLAVELL, RA
白介素 1 β (IL-1 β) 转换酶 (ICE) 将无活性的 IL-1 β 前体加工成促炎细胞因子。带有破坏的 ICE 基因 (ICE(-/-)) 的小鼠的贴壁单核细胞在脂多糖刺激后不会输出 IL-1 β 或白细胞介素 1 α (IL-1 α)。这些细胞输出的肿瘤坏死因子-α 和白细胞介素-6 (IL-6) 也减少了。 ICE(-/-)小鼠胸腺细胞对地塞米松或电离辐射诱导的细胞凋亡敏感，但对Fas抗体诱导的细胞凋亡具有抵抗力。尽管存在细胞凋亡缺陷，ICE(-/-) 小鼠仍能正常发育。
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.