Postischemic reperfusion injury to allografts: its impact on T-cell alloactivation via upregulation of dendritic cell–mediated stimulation, co-stimulation, and adhesion

Accumulating experimental and clinical data suggest that postischemic reperfusion injury to allografts has a major role—mediated by reactive oxygen species—in the initiation of alloimmune responsiveness. This nonspecific injury contributes to T-cell alloactivation via the activation of dendritic cells, which were recently recognized as the regulators and modulators of immunity. The reperfusion injury–upregulated expression of major histocompatibility complex products, co-stimulatory molecules, and adhesion molecules on dendritic cells may be underlying mechanisms. Reperfusion injury may facilitate communication among dendritic cells and T cells and the travel of these cells into and out of the graft, leading to the disintegration of the donor organ’s vessel walls. Dendritic cells and T cells may meet either in the allograft itself or the lymphoid tissue.