Describe the process of graft rejection in transplantation Essay

Describe the process of graft rejection in transplantation - Essay Example tegorized by thrombotic occlusions and haemorrhage of the graft vasculature occurs as a result of pre-existing host antibodies that remain bonded to antigens found in the graft  endothelium. The complement system gets activated through the recognition of the antigens, accompanied by invasion of neutrophils. Coagulation is initiated by the lipid particles that are discarded from the endothelial cells and platelets. The graft gets vascularised through the inflammation that occurs and the graft suffers irreparable damage (Graft Rejection, n.d.). Acute rejections are common in transplants and usually occur by incompatible HLA antigens found in the cells. T-cells are involved in rejections that result in the production of cytokines by the graft cells that engage other inflammatory cells in the process, and cause necrosis of allograft tissues. In chronic rejections occlusions are visible in graft arteries that are caused by the smooth muscle cells that proliferate and the fibroblasts that produce collagens. This process is known as accelerated or graft arteriosclerosis and that causes fibrosis and can lead to ischemia and cell death (Graft Rejection, n.d.). Sensitization and Effector are the two primary stages of the process of the graft rejection process in transplantation. In the sensitization stage, the CD4 and CD8 categories of T-cells use their receptors and identify the alloantigens that are present on the foreign graft cells. The signals required for the process are provided by the interactions between the T-cell receptor and antigen, and co-stimulatory receptor/ligand with T-cell or APC regulator. Peptide-binding grooves are formed by the helices of MHC molecules and these are made in use by the peptides derived from normal cellular proteins. Direct and indirect pathways of allorecognition cause the production of diverse sets of allospecific clones of T-cell (Malhotra, 2011). The effector mechanisms are supported by the Alloantigen-dependent and independent