Role of complement and NK cells in antibody mediated rejection.
Role of complement and NK cells in antibody mediated rejection.
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DOI：
10.1016/j.humimm.2012.07.330
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发表时间：
2012-12
期刊：
影响因子：
2.7
通讯作者：
Colvin, Robert B.
中科院分区：
文献类型：
--
作者：
Akiyoshi, Takurin;Hirohashi, Tsutomu;Alessandrini, Alessandro;Chase, Catherine M.;Farkash, Evan A.;Smith, R. Neal;Madsen, Joren C.;Russell, Paul S.;Colvin, Robert B.
尽管对T细胞和针对细胞介导的排斥反应的有效免疫抑制方案进行了广泛的研究，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。C4d在移植物中的沉积已被证明是一个有用的AMR标记；然而，C4d与AMR之间存在不完全关联。虽然补体被认为是急性AMR的主要参与者，但其在慢性AMR中的作用机制仍存在争议。最近的研究支持NK细胞的作用和抗体对内皮细胞的直接作用，表明存在补体非依赖性途径。在此，我们回顾了实验动物研究的历史，目前可用的系统和进展。尽管人类和动物研究的结果一致，但由于物种之间内皮功能的差异，将实验结果从啮齿动物转移到人类一直受到阻碍。我们简要描述患者的发现，并将其与动物的结果进行比较，以提出一个综合的观点。
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.
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影响因子：
19.6
作者：
通讯作者：
--
影响因子：
41.5
作者：
Farkash, Evan A.;Colvin, Robert B.
通讯作者：
Colvin, Robert B.
影响因子：
8.8
作者：
Einecke, G.;Sis, B.;Halloran, P. F.
通讯作者：
Halloran, P. F.
影响因子：
15.3
作者：
Arase, N;Arase, H;Saito, T
通讯作者：
Saito, T
影响因子：
6.2
作者：
HALLORAN, PF;WADGYMAR, A;SRINIVASA, NS
通讯作者：
SRINIVASA, NS