[Sterile inflammatory response to ischemia-reperfusion injury: immediate and long term consequences on graft function].

Solid organs used for transplantation are subjected to ischemia-reperfusion, which induces cellular stress and tissue necrosis. Ischemia-reperfusion injury activates the complement cascade and triggers the release of danger-associated molecular signals. The latter bind to pattern-recognition receptors on innate immune cells, thereby eliciting a sterile inflammatory response that, together with complement activation, increases tissue damage. This sterile inflammatory response also triggers maturation of antigen-presenting cells (macrophages and dendritic cells), enabling them to present donor antigens efficiently to recipient lymphocytes. By initiating adaptive alloimmune responses in the recipient, innate immunity plays a central role in the rejection process, which remains a major cause of late graft failure. Strategies capable of dampening the sterile inflammatory response induced by ischemia-reperfusion could therefore be beneficial, both for immediate post-transplantation graft function and for long-term outcome.