pISSN 2671-8790 eISSN 2671-8804

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Review Article

J Korean Soc Transplant 2017; 31(3): 99-110

Published online September 30, 2017

https://doi.org/10.4285/jkstn.2017.31.3.99

© The Korean Society for Transplantation

Immunologic Mechanism of Ischemia Reperfusion Injury in Transplantation

Jong Soo Lee, M.D.1,2

Division of Nephrology, Department of Internal Medicine, Ulsan University Hospital, University of Ulsan College of Medicine1, Biomedical Research Center2, Ulsan, Korea

Correspondence to: Jong Soo Lee
Division of Nephrology, Department of Internal Medicine, Ulsan University Hospital, University of Ulsan College of Medicine, 877 Bangeojinsunhwan-doro, Dong-gu, Ulsan 44033, Korea
Tel: 82-52-250-8843, Fax: 82-52-251-8235 E-mail: jslee@uuh.ulsan.kr

Received: September 5, 2017; Accepted: September 6, 2017

Abstract

Ischemia-reperfusion injury (IRI) is an inevitable consequence of organ transplantation that has major consequences for graft-and patient survival. During transplantation procedures, allografts are exposed to various periods of complete ischemia. Ischemic insult starts with brain death, and its associated hemodynamic disturbances continue during donor organ procurement, cold preservation, and implantation. Ischemia-reperfusion injury, which is a risk factor for acute graft injury, delayed graft function, and acute and chronic rejection, is triggered following reperfusion. Along the cascade of pathogenic events that accompany ischemic insults and cause IRI, there has been an appreciation for various immune mechanisms within the allograft itself. The pathophysiological events associated with IRI originate in signals derived from pattern recognition receptors (PRRs) expressed in the donor organ. Danger associated molecular patterns (DAMP) released from injured cells serve as ligands for PRRs expressed on many cells in the donor organ. Activation of PRR signaling in the donor organ leads to production of proinflammatory cytokines and activates the innate immune system, triggering adaptive immune responses as well as cell death signaling, ultimately worsening the initial ischemic injury. Accordingly, deciphering the inflammatory pathway of innate immunity in IRI may provide a good therapeutic target to block acute sterile inflammation caused by tissue damage.

Keywords: Transplantation, Innate immunity, Inflammation