Innate Immune Regulations and Liver Ischemia-Reperfusion Injury.
Innate Immune Regulations and Liver Ischemia-Reperfusion Injury.
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DOI：
10.1097/tp.0000000000001411
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发表时间：
2016-12
期刊：
影响因子：
6.2
通讯作者：
Zhai Y
中科院分区：
文献类型：
--
作者：
Lu L;Zhou H;Ni M;Wang X;Busuttil R;Kupiec-Weglinski J;Zhai Y
肝脏缺血再灌注激活天然免疫系统，促使炎性肝细胞损伤的全面发展。损伤相关分子模式（DAMP）通过模式识别受体（PRR）刺激骨髓和树突状细胞以启动免疫应答。复杂的细胞内信号传导网络转导炎症信号以调节先天免疫细胞活化和实质细胞死亡。最近的研究表明，DAMPs不仅可以触发促炎反应，还可以通过激活不同的PRR或独特的细胞内信号通路或在特殊的细胞群中触发免疫调节反应。此外，组织损伤环境激活也调节炎性疾病过程的PRR非依赖性受体。因此，肝脏IRI的先天免疫机制涉及不同的分子和细胞相互作用，在不同的细胞中受到内源性和外源性调节。更好地理解这些复杂的调控通路/网络对于我们设计安全有效的治疗策略以改善患者的肝脏IRI是至关重要的。
Liver ischemia reperfusion activates innate immune system to drive the full development of inflammatory hepatocellular injury. Damage-associated molecular patterns (DAMPs) stimulate myeloid and dendritic cells via pattern recognition receptors (PRRs) to initiate the immune response. Complex intracellular signaling network transduces inflammatory signaling to regulate both innate immune cell activation and parenchymal cell death. Recent studies have revealed that DAMPs may trigger not only proinflammatory, but also immune regulatory responses by activating different PRRs or distinctive intracellular signaling pathways or in special cell populations. Additionally, tissue injury milieu activates PRR-independent receptors which also regulate inflammatory disease processes. Thus, the innate immune mechanism of liver IRI involves diverse molecular and cellular interactions, subjected to both endogenous and exogenous regulation in different cells. A better understanding of these complicated regulatory pathways/network is imperative for us in designing safe and effective therapeutic strategy to ameliorate liver IRI in patients.