Department of Pathology, Harvard Medical School, Massachusetts General Hospital, Boston, MA 02114, USA.
Hum Immunol. 2012 Dec;73(12):1226-32. doi: 10.1016/j.humimm.2012.07.330. Epub 2012 Jul 28.
Despite extensive research on T cells and potent immunosuppressive regimens that target cellular mediated rejection, few regimens have been proved to be effective on antibody-mediated rejection (AMR), particularly in the chronic setting. C4d deposition in the graft has been proved to be a useful marker for AMR; however, there is an imperfect association between C4d and AMR. While complement has been considered as the main player in acute AMR, the effector mechanisms in chronic AMR are still debated. Recent studies support the role of NK cells and direct effects of antibody on endothelium cells in a mechanism suggesting the presence of a complement-independent pathway. Here, we review the history, currently available systems and progress in experimental animal research. Although there are consistent findings from human and animal research, transposing the experimental results from rodent to human has been hampered by the differences in endothelial functions between species. We briefly describe the findings from patients and compare them with results from animals, to propose a combined perspective.
尽管针对 T 细胞和强效免疫抑制方案进行了广泛的研究，以靶向细胞介导的排斥反应，但很少有方案被证明对抗体介导的排斥反应（AMR）有效，特别是在慢性情况下。在移植物中沉积 C4d 已被证明是 AMR 的有用标志物；然而，C4d 与 AMR 之间的关联并不完美。虽然补体被认为是急性 AMR 的主要参与者，但慢性 AMR 的效应机制仍存在争议。最近的研究支持 NK 细胞和抗体对内皮细胞的直接作用在一种机制中的作用，该机制表明存在补体非依赖性途径。在这里，我们回顾了历史、当前可用的系统和实验动物研究的进展。尽管人类和动物研究有一致的发现，但由于物种间内皮功能的差异，将啮齿动物的实验结果转化为人类的研究受到了阻碍。我们简要描述了患者的发现，并将其与动物的结果进行了比较，提出了一个综合的观点。
