Abstract
Platelet-activating factor is a phospholipid mediator of inflammation produced both by inflammatory cells (e.g., basophils, neutrophils, monocytes, platelets) and endothelial cells (1); its production is stimulated by several cytokine mediators, including TNF. The role of PAF in allograft rejection includes increasing endothelial permeability leading to reduced blood flow and margination of leukocytes; recruitment of cells into the allograft at the initiation of rejection; and intercellular signaling within the graft (2–4). In vivo evidence of PAF's role in rejection comes from a rabbit model, where a sustained local release of PAF was observed during hyperacute renal allograft rejection, with associated platelet and neutrophil accumulation within 5 min of revascularization (5).
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