Actors involved
Mechanism
Where?
In the transplanted organ.
When?
At the time of transplantation, as soon as the anastomoses are made and the “no reflow” period has passed.
It is often associated with a haemostasis disorder (platelet aggregation).
How is this done?
Consequences
It is difficult to distinguish the phenomena of ischaemia and reperfusion because their consequences on the outcome of the graft are closely linked. In fact, the lesions induced by ischaemia, such as the release of DAMP and endothelial activation will be highlighted and increased by the recruitment of leukocytes during reperfusion.
The release of DAMP by injured cells generates an innate immune response. Numerous dendritic cells and macrophages will be recruited via their TLR, activated and migrate into the lymph nodes draining the transplanted organ to initiate the adaptive immune response via the activation of T and B cells.
The greater the innate response caused by ischaemia/reperfusion, the greater the risks of an adaptive response causing acute and/or chronic rejections. Many strategies are being studied to improve the conditions for preserving the removed organ in order to minimise damage during this perioperative period of transplantation.