Zimmerman Michael A, Martin Alicia, Yee Jennifer, Schiller Jennifer, Hong Johnny C
Department of Surgery, Division of Transplant Surgery, Medical College of Wisconsin, Milwaukee, WI 53226, USA.
Histocompatibility and Immunogenetics, Blood Center of Wisconsin, Milwaukee, WI 53201, USA.
J Clin Med. 2017 Apr 1;6(4):41. doi: 10.3390/jcm6040041.
Restoration of blood flow to an ischemic organ results in significant tissue injury. In the field of liver transplantation, ischemia-reperfusion injury (IRI) has proven to be a formidable clinical obstacle. In addition to metabolic stress and inflammation, IRI results in profound graft dysfunction and loss. The severity of IRI further limits the ability to expand the donor pool by using partial grafts and marginal organs. As such, the inflammatory response to reperfusion of the liver continues to be an area of intense investigation. Among the various leukocytes involved in IRI, new insights suggest that natural killer T (NKT) cells may be a central driver of hepatocellular injury. Herein, we examine recent experimental observations that provide a mechanistic link between NKT cell recruitment to liver and post-perfusion tissue injury.
恢复缺血器官的血流会导致显著的组织损伤。在肝移植领域，缺血再灌注损伤（IRI）已被证明是一个巨大的临床障碍。除了代谢应激和炎症外，IRI还会导致严重的移植物功能障碍和丧失。IRI的严重程度进一步限制了通过使用部分移植物和边缘器官来扩大供体库的能力。因此，肝脏再灌注的炎症反应仍然是一个深入研究的领域。在参与IRI的各种白细胞中，新的见解表明自然杀伤T（NKT）细胞可能是肝细胞损伤的核心驱动因素。在此，我们研究了最近的实验观察结果，这些结果提供了NKT细胞募集到肝脏与灌注后组织损伤之间的机制联系。
