Department of Surgery, Washington University in St Louis, St. Louis, MO, USA.
Transpl Int. 2013 Jan;26(1):2-10. doi: 10.1111/j.1432-2277.2012.01549.x. Epub 2012 Aug 21.
Ischemia reperfusion injury (IRI) that occurs with solid organ transplantation activates the innate immune system to induce inflammation. This leads to enhanced acute allograft rejection, impaired transplant tolerance and accelerated progression of chronic rejection. In this review, we discuss the innate immune signaling pathways that have been shown to play a role in organ transplantation. In particular, we focus on Toll-like receptor signaling pathways and how they have influenced outcomes after organ transplantation both experimentally and from clinical studies. Furthermore, we describe the substances that trigger the innate immune system after transplantation and several of the key cellular mediators of inflammation. We specifically point out unique aspects of activation of the innate immune system after lung transplantation. Finally, we discuss the areas that should be investigated in the future to more clearly understand the influence of the innate immune system after organ transplantation.
缺血再灌注损伤(IRI)发生在实体器官移植中,激活固有免疫系统引发炎症。这导致急性移植物排斥反应增强、移植耐受受损和慢性排斥反应加速进展。在这篇综述中,我们讨论了已被证明在器官移植中起作用的固有免疫信号通路。特别是,我们关注 Toll 样受体信号通路,以及它们如何在实验和临床研究中影响器官移植后的结果。此外,我们描述了移植后触发固有免疫系统的物质和炎症的几个关键细胞介质。我们特别指出了肺移植后固有免疫系统激活的独特方面。最后,我们讨论了未来应该研究的领域,以更清楚地了解器官移植后固有免疫系统的影响。