Abstract
Antibody-mediated rejection (AMR) has been identified as a main obstacle for stable immune tolerance and long survival of kidney allografts. In spite of new insights into the underlying mechanisms of AMR, accurate diagnosis and efficient treatment are still challenges in clinical practice. Endothelium is the first barrier between recipients' immune systems and grafts in vascularized organ transplants. Considering that endothelial cells express a number of antigens that can be attacked by various allo- and autoantibodies, endothelial cells act as main targets for the recipients' humoral immune responses. Importantly, emerging evidence has shown that endothelial cells in transplants could also initiate protective mechanisms in response to immune injuries. A better understanding of the role of endothelial cells during the pathogenesis of AMR might provide novel therapeutic targets. In the present review, we summarize the antigens expressed by endothelial cells and also discuss the activation and accommodation of endothelial cells as well as their clinical implications. Collectively, the progress discussed in this review indicates endothelial cells as promising targets to improve current diagnosis and therapeutic regimens for AMR.
Highlights
Cell-mediated rejection (CMR) was recognized as the predominant form of immune response in organ transplantation
As endothelial cells express a number of antigens that can be targeted by various allo- and autoantibodies (Abs), endothelial cells play an important role in the pathogenesis of antibody-mediated rejection (AMR) [3,4,5]
Preformed anti-Human Leukocyte Antigens (HLA) donor-specific antibodies (DSAs) due to pregnancies, blood transfusions, and organ transplantation contribute to higher risk for AMR and allograft failure [14]
Summary
Cell-mediated rejection (CMR) was recognized as the predominant form of immune response in organ transplantation. Progress in the last decade suggested that, besides CMR, antibody-mediated rejection (AMR) significantly contributes to the rejection and pathogenesis of allografts [1, 2]. Despite the substantial advances in understanding the pathologic process of AMR, accurate diagnosis and efficient treatment are still challenges in clinic. This could be partly ascribed to our limited knowledge of the underlying mechanisms of AMR. This review will summarize the cross talk between endothelial cells and antibodies in allograft rejection and its clinical relevance. We will discuss the mechanism of activation and accommodation of endothelial cells and their clinical implications.
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