Organ preservation injury and innate immunity

Abstract

Purpose of review Organ preservation injury involves complex molecular pathways and cellular interactions that ultimately lead to transplant damage, delayed function, or ultimate failure. This review focuses on the role of two major components of innate immunity in the context of ischemia–reperfusion injury: the Toll-like receptor and the complement system. Recent findings Advances in the pathophysiology of liver ischemia–reperfusion injury have further demonstrated the importance of the Toll-like receptor system in mediating the innate immune response. Functional Toll-like receptor 4 signaling on phagocytic nonparenchymal cells has been shown to be essential in the pathophysiology of liver ischemia–reperfusion injury. A novel mechanism of innate immune-induced T-cell recruitment and function has been demonstrated in the context of CXCR3 chemokine biology. In addition, the pharmacological inhibition of the complement system appears effective in reducing liver ischemia–reperfusion injury, suggesting its possible role in clinical applications. Summary Despite advances in our appreciation of the putative mechanisms involved with innate immune activation during organ ischemia–reperfusion injury, many details of these complex molecular events remain unknown. Additional comprehensive research is warranted to elucidate the pathogenesis of organ preservation injury in the context of the innate immune system.