title: Innate Immune Regulations and Liver Ischemia-Reperfusion Injury.
abstract: 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 ischemia-reperfusion injury 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 ischemia-reperfusion injury in patients.
authors.affiliation: 1 Dumont-UCLA Transplant Center, Division of Liver and Pancreas Transplantation, Department of Surgery, David Geffen School of Medicine at University of California-Los Angeles, Los Angeles, CA. 2 Liver Transplantation Center, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu Province, China.
authors.forename: Ling
authors.initials: L
authors.lastname: Lu
authors.forename: Haoming
authors.initials: H
authors.lastname: Zhou
authors.forename: Ming
authors.initials: M
authors.lastname: Ni
authors.forename: Xuehao
authors.initials: X
authors.lastname: Wang
authors.forename: Ronald
authors.initials: R
authors.lastname: Busuttil
authors.forename: Jerzy
authors.initials: J
authors.lastname: Kupiec-Weglinski
authors.forename: Yuan
authors.initials: Y
authors.lastname: Zhai
mesh_terms: D000818:Animals; D003713:Dendritic Cells / Q000166:cytology; D024243:HMGB1 Protein / Q000378:metabolism; D006801:Humans; D007113:Immunity, Innate; D007155:Immunologic Factors / Q000276:immunology*; D007249:Inflammation; D007372:Interferons / Q000378:metabolism; D007511:Ischemia; D008099:Liver / Q000473:pathology*; D051379:Mice; D022423:Myeloid Cells / Q000166:cytology; D051192:Receptors, Pattern Recognition / Q000276:immunology*; D015427:Reperfusion Injury / Q000276:immunology*; D015398:Signal Transduction; D051197:Toll-Like Receptor 4 / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D024243:HMGB1 Protein; C585491:HMGB1 protein, human; D007155:Immunologic Factors; D051192:Receptors, Pattern Recognition; C495345:TLR4 protein, human; D051197:Toll-Like Receptor 4; D014409:Tumor Necrosis Factor-alpha; D007372:Interferons