Sedmak D D, Knight D A, Vook N C, Waldman J W
Department of Pathology, Ohio State University College of Medicine, Columbus.
Transplantation. 1994 Dec 27;58(12):1379-85.
Endothelial cells, one of several in vivo host cells for cytomegalovirus (CMV), participate in solid organ allograft rejection in part through the expression of leukocyte adhesion molecules. The hypothesis that CMV infection alters the constitutive and induced expression of ELAM-1, ICAM-1, and VCAM-1 on infected human umbilical vein endothelial cells (HUVECs) was examined. HUVECs were infected with an endothelial cell-propagated strain of CMV (VHL/E) for various periods, treated with tumor necrosis factor-alpha (TNF alpha), and examined by flow cytometry or immunohistochemically dual-labeled with monoclonal antibodies to CMV immediate early nuclear protein and ELAM-1, ICAM-1, or VCAM-1. Neither ELAM-1 nor VCAM-1 was induced on CMV-infected HUVECs, and treatment with TNF alpha treatment did not result in their induction. In contrast, ICAM-1 was induced on infected HUVECs by 24 hr postinfection. Endothelial ICAM-1 induction may represent a mechanism by which CMV infection exacerbates the recipient cellular immune response to allografts.
内皮细胞是巨细胞病毒（CMV）在体内的几种宿主细胞之一，部分通过白细胞粘附分子的表达参与实体器官同种异体移植排斥反应。本研究检验了CMV感染会改变感染的人脐静脉内皮细胞（HUVECs）上ELAM-1、ICAM-1和VCAM-1的组成性表达和诱导性表达这一假说。将HUVECs用内皮细胞增殖的CMV株（VHL/E）感染不同时间，用肿瘤坏死因子-α（TNFα）处理，然后通过流式细胞术进行检测，或用针对CMV立即早期核蛋白以及ELAM-1、ICAM-1或VCAM-1的单克隆抗体进行免疫组织化学双重标记检测。在CMV感染的HUVECs上，ELAM-1和VCAM-1均未被诱导，用TNFα处理也未导致它们被诱导。相比之下，感染后24小时，ICAM-1在受感染的HUVECs上被诱导。内皮ICAM-1的诱导可能代表了一种机制，通过该机制CMV感染加剧了受体对同种异体移植物的细胞免疫反应。
