Immunologic Mechanism of Ischemia Reperfusion Injury in Transplantation.
10.4285/jkstn.2017.31.3.99
- Author:
Jong Soo LEE
1
Author Information
1. Division of Nephrology, Department of Internal Medicine, Ulsan University Hospital, University of Ulsan College of Medicine, Ulsan, Korea. jslee@uuh.ulsan.kr
- Publication Type:Review
- Keywords:
Transplantation;
Innate immunity;
Inflammation
- MeSH:
Allografts;
Brain Death;
Cell Death;
Cytokines;
Delayed Graft Function;
Hemodynamics;
Humans;
Immune System;
Immunity, Innate;
Inflammation;
Ischemia*;
Ligands;
Organ Transplantation;
Porcine Reproductive and Respiratory Syndrome;
Receptors, Pattern Recognition;
Reperfusion;
Reperfusion Injury*;
Risk Factors;
Tissue and Organ Procurement;
Tissue Donors;
Transplantation;
Transplants
- From:The Journal of the Korean Society for Transplantation
2017;31(3):99-110
- CountryRepublic of Korea
- Language:Korean
-
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.
