Toll-like receptor signaling in cell proliferation and survival.
Toll-like receptor signaling in cell proliferation and survival.
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DOI：
10.1016/j.cyto.2009.08.010
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发表时间：
2010-01
期刊：
影响因子：
3.8
通讯作者：
Tapping, Richard I.
中科院分区：
文献类型：
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作者：
Li, Xinyan;Jiang, Song;Tapping, Richard I.
Toll 样受体 (TLR) 是外来微生物成分以及受损或发炎的自身组织产物的重要传感器。在感应到这些分子后，TLR 启动一系列下游信号传导事件，驱动细胞反应，包括细胞因子、趋化因子和其他炎症介质的产生。这一结果是由驱动磷酸化和其他信号级联的蛋白质复合物的细胞内组装产生的，最终导致染色质重塑和转录因子激活。除了驱动炎症反应外，TLR 还调节细胞增殖和存活，从而扩大有用的免疫细胞并整合炎症反应和组织修复过程。在这种情况下，中央 TLR 信号分子，例如丝裂原激活蛋白激酶 (MAPK) 和磷酸肌醇 3-激酶 (PI3K)，发挥着关键作用。此外，作为 TLR 激活目标的四类主要转录因子也控制着细胞命运。本综述重点关注 TLR 信号传导在细胞增殖和存活中的作用。该主题不仅对于了解宿主防御和组织修复具有重要意义，而且对于通常与慢性炎症相关的癌症也具有重要意义。
Toll-like receptors (TLRs) are important sensors of foreign microbial components as well as products of damaged or inflamed self tissues. Upon sensing these molecules, TLRs initiate a series of downstream signaling events that drive cellular responses including the production of cytokines, chemokines and other inflammatory mediators. This outcome results from the intracellular assembly of protein complexes that drive phosphorylation and other signaling cascades ultimately leading to chromatin remodeling and transcription factor activation. In addition to driving inflammatory responses, TLRs also regulate cell proliferation and survival which serves to expand useful immune cells and integrate inflammatory responses and tissue repair processes. In this context, central TLR signaling molecules, such as the mitogen-activated protein kinases (MAPK) and phosphoinositide 3-kinase (PI3K), play key roles. In addition, four major groups of transcription factors which are targets of TLR activation also control cell fate. This review focuses on the role of TLR signaling as it relates to cell proliferation and survival. This topic not only has important implications for understanding host defense and tissue repair, but also cancer which is often associated with conditions of chronic inflammation.
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