由白细胞介素-1β转化酶介导的干扰素-γ诱导因子的激活。
Activation of interferon-gamma inducing factor mediated by interleukin-1beta converting enzyme.
作者信息
Gu Y, Kuida K, Tsutsui H, Ku G, Hsiao K, Fleming M A, Hayashi N, Higashino K, Okamura H, Nakanishi K, Kurimoto M, Tanimoto T, Flavell R A, Sato V, Harding M W, Livingston D J, Su M S
机构信息
Vertex Pharmaceuticals, Inc., 130 Waverly Street, Cambridge, MA 02139, USA.
出版信息
Science. 1997 Jan 10;275(5297):206-9. doi: 10.1126/science.275.5297.206.
The interleukin-1beta (IL-1beta) converting enzyme (ICE) processes the inactive IL-1beta 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.
白细胞介素-1β（IL-1β）转化酶（ICE）可将无活性的IL-1β前体加工成促炎细胞因子。研究还表明，ICE能在真正的加工位点高效切割干扰素-γ诱导因子（IGIF）的前体，从而激活IGIF并促进其分泌。脂多糖激活的ICE缺陷型（ICE-/-）库普弗细胞能合成IGIF前体，但无法将其加工成活性形式。在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水平降低。ICE-/-小鼠缺乏多种促炎细胞因子，这可能是它们免受脓毒性休克的原因。
Zotero 插件