Activation of interferon-gamma inducing factor mediated by interleukin-1 beta converting enzyme
Activation of interferon-gamma inducing factor mediated by interleukin-1 beta converting enzyme
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DOI：
10.1126/science.275.5297.206
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发表时间：
1997-01-10
期刊：
影响因子：
56.9
通讯作者：
Su, MSS
中科院分区：
文献类型：
--
作者：
Gu, Y;Kuida, K;Su, MSS
白介素1β(IL-1β)转换酶(ICE)处理致炎细胞因子的非活性IL-IP前体。ICE还被证明在真正的加工部位高效地切割干扰素-γ诱导因子(IGIF)的前体，从而激活IGIF并促进其输出。内毒素激活的ICE缺陷型(ICE(-/-))Kupffer细胞合成IGIF前体，但不能将其加工成活性形式。暴露于痤疮丙酸杆菌和脂多糖的ICE(-/-)小鼠血清中干扰素-γ和IGIF均降低。ICE(-/-)小鼠缺乏多种促炎细胞因子可能是其对感染性休克具有保护作用的原因。
The interleukin-1 beta (IL-1 beta) converting enzyme (ICE) processes the inactive IL-IP precursor to the proinflammatory cytokine. ICE was also shown to cleave the precursor of interferon-gamma inducing factor (IGIF) at the authentic processing site with high efficiency, thereby activating IGIF and facilitating its export. Lipopolysaccharide-activated ICE-deficient (ICE(-/-)) Kupffer cells synthesized the IGIF precursor but failed to process it into the active form. Interferon-gamma and IGIF were diminished in the sera of ICE(-/-) mice exposed to Propionibacterium acnes and lipopolysaccharide. The lack of multiple proinflammatory cytokines in ICE(-/-) mice may account for their protection from septic shock.