Knight D A, Waldman W J, Sedmak D D
Department of Pathology, Ohio State University College of Medicine and Public Health, Columbus 43210-1218, USA.
Transplantation. 1999 Dec 15;68(11):1814-8. doi: 10.1097/00007890-199912150-00030.
Cytomegalovirus (CMV), a betaherpesvirus associated with allograft rejection, infects the endothelium, the cellular interface between allograft tissue and the host immune system. Because of recent appreciation of the phenotypic diversity of endothelial cells (EC) from different vascular compartments, controversy now exists on the universality of CMV-mediated adhesion molecule induction previously described on umbilical vein EC. Therefore, we herein extend these previous studies to arterial and microvascular EC, which represent sites of vascular rejection.
Human coronary artery, aortic, umbilical artery, and microvascular EC were mock or CMV infected and/or treated with tumor necrosis factor-a before flow cytometric and immunohistochemical analysis.
CMV directly enhanced intercellular adhesion molecule-1 on all EC isolates but did not induce E-selectin or vascular cell adhesion molecule-1. Furthermore, CMV-infected EC were refractory to tumor necrosis factor-alpha-mediated induction of these molecules.
CMV-induced modulations of adhesion molecule expression, which may affect allograft immunogenicity, seem common to all EC regardless of vascular origin.
巨细胞病毒（CMV）是一种与同种异体移植排斥反应相关的β疱疹病毒，它感染内皮细胞，即同种异体移植组织与宿主免疫系统之间的细胞界面。由于最近认识到来自不同血管腔室的内皮细胞（EC）的表型多样性，先前在脐静脉EC上描述的CMV介导的黏附分子诱导的普遍性现在存在争议。因此，我们在此将这些先前的研究扩展到动脉和微血管EC，它们代表血管排斥反应的部位。
在进行流式细胞术和免疫组织化学分析之前，将人冠状动脉、主动脉、脐动脉和微血管EC进行模拟或CMV感染和/或用肿瘤坏死因子-α处理。
CMV直接增强了所有EC分离株上的细胞间黏附分子-1，但未诱导E-选择素或血管细胞黏附分子-1。此外，CMV感染的EC对肿瘤坏死因子-α介导的这些分子的诱导具有抗性。
CMV诱导的黏附分子表达调节可能影响同种异体移植的免疫原性，似乎对所有EC都是常见的，无论其血管来源如何。
