Innate Immunity - Professor Richard Kirk 2023

Innate immunity is usually only thought of in protecting from non HLA pathogens e.g. viruses, bacteria, however it is intimately involved with inflammation. Organ damage occurs at the time of brain stem death due to a hormonal and cytokine storm, followed by ischemic-reperfusion injury and thermal injury as organs are usually transported at 4°C. On implant of the donor organ the innate system has a major part to play in removing apoptotic cells and debris.

Increasingly however the interplay between the innate and adaptive immune system is being recognised in rejection. When rejection occurs there is cell damage and apoptosis. Cells and cytokines of the innate system ae able to promote or downplay the resulting inflammation. The various components and effector functions  of the innate system are shown in Figure 1 and in more detail in this table.

Tissue damage causes the release of components (e.g. histamine, pro-inflammatory cytokines and chemokines) from endothelial cells as  well as by cells in the graft tissue such as mast cells and innate lymphoid cells which  have the ability to induce chemotaxis and allow interaction between  leukocytes and endothelium and the subsequent leukocyte transmigration  at the site of the injury. The cell migration process is complex, usually first by neutrophils and then by monocytes. If  the ongoing rejection is not stopped then inflammation may continue with further graft damage which may be irreversible.