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Monitoring Changes in Human Umbilical Vein Endothelial Cells upon Viral Infection Using Impedance-Based Real-Time Cell Analysis
Published on: May 5, 2023
The role of vascular endothelial cells in transplantation
1Department of Pathology, Ohio State University, Columbus 43210.
The interface between an allograft and the recipient's immune system is the endothelium of the allograft vasculature. In this boundary position, endothelial cells may play important roles in the afferent and efferent phases of allograft rejection, in the response of the allograft to pretransplant perfusion and to drug therapy, and in the response to viral infection of the host. The expression by endothelial cells of granule membrane protein-140 (GMP-140) and endothelial leukocyte adhesion molecule-1 (ELAM-1), increased tissue factor activity, increased secretion of plasminogen activator inhibitor, and decreased thrombomodulin may all contribute to hyperacute rejection. Similarly, endothelial cells may actively participate in acute cellular rejection and in the development of transplant-associated arteriopathy as a result of induction of antigen-presenting function (ie, HLA class II expression), upregulation of adhesion molecules for lymphocytes and monocytes, and release of platelet-derived growth factors. Endothelial cell functions, which are important for normal inflammatory responses and vessel behavior, may be pathogenic in the allograft.
The interface between an allograft and the recipient's immune system is the endothelium of the allograft vasculature. In this boundary position, endothelial cells may play important roles in the afferent and efferent phases of allograft rejection, in the response of the allograft to pretransplant perfusion and to drug therapy, and in the response to viral infection of the host. The expression by endothelial cells of granule membrane protein-140 (GMP-140) and endothelial leukocyte adhesion molecule-1 (ELAM-1), increased tissue factor activity, increased secretion of plasminogen activator inhibitor, and decreased thrombomodulin may all contribute to hyperacute rejection. Similarly, endothelial cells may actively participate in acute cellular rejection and in the development of transplant-associated arteriopathy as a result of induction of antigen-presenting function (ie, HLA class II expression), upregulation of adhesion molecules for lymphocytes and monocytes, and release of platelet-derived growth factors. Endothelial cell functions, which are important for normal inflammatory responses and vessel behavior, may be pathogenic in the allograft.
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