Collins A D, Ationu A
Department of Biochemistry and Molecular Biology, University of Leeds, Leeds, LS2 9JT, UK.
Int J Mol Med. 1998 Feb;1(2):439-52. doi: 10.3892/ijmm.1.2.439.
Transplant coronary artery disease (TxCAD) is manifest as a diffuse, concentric intimal proliferation which results in occlusion of the allograft vessel lumen, and is responsible for limiting the long-term success of cardiac transplantation. The recent discovery of high circulating levels of anti-endothelial antibodies (AEAs) in patients with TxCAD has resulted in increased clinical and experimental research interests in understanding their patho-physiological roles in TxCAD. Increasing evidence suggests that AEAs are cross-reactive towards an endothelial protein doublet of 56-58 kDa which has now been characterised and identified as the cytoskeletal protein vimentin. Despite this recent progress the immunopathogenesis of TxCAD remains unclear. In this review recent developments and mechanisms of the involvement of AEAs in the immunopathogenesis of TxCAD are discussed.
移植冠状动脉疾病（TxCAD）表现为弥漫性、同心性内膜增生，导致移植血管腔闭塞，是限制心脏移植长期成功的原因。最近发现TxCAD患者循环中抗内皮抗体（AEA）水平升高，这使得在了解其在TxCAD中的病理生理作用方面，临床和实验研究兴趣增加。越来越多的证据表明，AEA与一种56 - 58 kDa的内皮蛋白双峰发生交叉反应，该蛋白现已被鉴定为细胞骨架蛋白波形蛋白。尽管有这一最新进展，但TxCAD的免疫发病机制仍不清楚。在这篇综述中，将讨论AEA参与TxCAD免疫发病机制的最新进展和机制。
