Antibody-mediated rejection: emergence of animal models to answer clinical questions.
Antibody-mediated rejection: emergence of animal models to answer clinical questions.
复制标题
DOI：
10.1111/j.1600-6143.2010.03065.x
复制
发表时间：
2010-05
期刊：
影响因子：
--
通讯作者：
Fairchild RL
中科院分区：
文献类型：
--
作者：
Baldwin WM 3rd;Valujskikh A;Fairchild RL
几十年的小动物实验已经打破了认为抗体是移植排斥反应的原因的观点，但临床经验，特别是致敏患者的经验，使基础免疫学家相信有必要开发模型来研究抗体介导的排斥反应(AMR)的潜在机制。这种重新燃起的兴趣导致了几种新的啮齿动物模型来研究抗体介导的心脏和肾移植损伤的机制，但令人满意的慢性AMR模型仍然难以获得。然而，这些新的研究已经开始揭示抗体与同种异体内皮结合的分子和病理后遗症。此外，抗体对血管内皮细胞的补体非依赖性和依赖性作用已在体外得到证实。随着小动物模型的更好定义，预计它们将被更广泛地用于回答有关抗体介导的组织损伤机制的进一步问题，以及设计治疗干预措施。
Decades of experiments in small animals had tipped the balance of opinion away from antibodies as a cause of transplant rejection, but clinical experience, especially with sensitized patients, has convinced basic immunologists of the need to develop models to investigate mechanisms underlying antibody-mediated rejection (AMR). This resurgent interest has resulted in several new rodent models to investigate antibody-mediated mechanisms of heart and renal allograft injury, but satisfactory models of chronic AMR remain more elusive. Nevertheless, these new studies have begun to reveal many insights into the molecular and pathological sequelae of antibody binding to the allograft endothelium. In addition, complement-independent and –dependent effects of antibodies on endothelial cells have been identified in vitro. As small animals models become better defined, it is anticipated that they will be more widely used to answer further questions concerning mechanisms of antibody-mediated tissue injury as well as to design therapeutic interventions.
登录
查看更多内容
影响因子：
8.8
作者：
Csencsits, K.;Burrell, B. E.;Bishop, D. K.
通讯作者：
Bishop, D. K.
影响因子：
20.1
作者：
Chatterjee TK;Stoll LL;Denning GM;Harrelson A;Blomkalns AL;Idelman G;Rothenberg FG;Neltner B;Romig-Martin SA;Dickson EW;Rudich S;Weintraub NL
通讯作者：
Weintraub NL
影响因子：
6.2
作者：
Brodsky, Sergey V.;Nadasdy, Gyongyi M.;Nadasdy, Tibor
通讯作者：
Nadasdy, Tibor
影响因子：
6.2
作者：
HALLORAN, PF;WADGYMAR, A;SRINIVASA, NS
通讯作者：
SRINIVASA, NS
影响因子：
8.8
作者：
Bickerstaffa, A.;Nozaki, T.;Fairchild, R. L.
通讯作者：
Fairchild, R. L.