Lipopolysaccharide signal transduction, regulation of tumor necrosis factor biosynthesis, and signaling by tumor necrosis factor itself
Lipopolysaccharide signal transduction, regulation of tumor necrosis factor biosynthesis, and signaling by tumor necrosis factor itself
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DOI：
10.1097/00005344-199500252-00002
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发表时间：
1995-01-01
影响因子：
3
通讯作者：
Kruys, V
中科院分区：
文献类型：
--
作者：
Beutler, B;Kruys, V
近年来，将细菌内毒素(脂多糖)引入哺乳动物宿主的一连串事件，以及随之而来的器官损伤和血管崩溃综合征，已经成为人们关注的焦点。几个与内毒素结合的分子，以及导致单核细胞释放细胞因子的信号级联的大致轮廓，已经被阐明。调节内毒素不良反应的主要细胞因子也已被确定。其中最重要的是肿瘤坏死因子(TNF)，它能引起几乎所有与其结合的细胞的生物反应。两种截然不同的受体负责转导肿瘤坏死因子信号。肿瘤坏死因子受体的作用机制正变得越来越清楚，我们有理由希望，通过多个不同层面的干预，内毒素的破坏性影响可能会减弱或避免。
In recent years, the chain of events that connects introduction of bacterial endotoxin (lipopolysaccharide; LPS) into a mammalian host, and the syndrome of organ damage and vascular collapse that ensues, have come into sharper focus. Several of the molecules that engage LPS, and a rough outline of the signaling cascade that leads to cytokine release from mononuclear cells, have been elucidated. The principal cytokines that mediate the untoward effects of LPS have also been identified. The most important of these is tumor necrosis factor (TNF), which elicits biologic responses from virtually every type of cell to which it binds. Two distinct receptors transduce the TNF signal. Mechanisms of TNF receptor action are becoming increasing clear, and there is reason to hope that, through intervention at many distinct levels, the devastating effects of LPS might be attenuated or averted.