Acute Rejection

Acute rejection is a process of injury to the graft parenchyma and blood vessels mediated by alloreactive T cells and antibodies. Before modern immunosuppres-sion, acute rejection would often begin several days to a few weeks after transplantation. The delayed time of onset of acute rejection is because alloreactive effector T cells and antibodies take time to be generated from naive or resting memory T cells in response to the graft. In current clinical practice, episodes of acute rejection may occur at much later times, even years after transplantation, if immunosuppression is reduced for any number of reasons. Although the patterns of acute rejection are divided into cellular, mediated by T cells, and patterns and mechanisms of allograft rejection 375

Hyperacute rejection

Endothelial cel

Hyperacute rejection

Alloantigen (e.g., blood group antigen)

Circulating alloantigen specific antibody

B Acute rejection

FIGURE 16-8 Immune mechanisms of graft rejection. A, In hyperacute rejection, preformed antibodies reactive with vascular endothelium activate complement and trigger rapid intravascular thrombosis and necrosis of the vessel wall. B, In acute rejection, CD8+ T lymphocytes reactive with alloantigens on endothelial cells and parenchymal cells mediate damage to these cell types. Alloreactive antibodies formed after engraftment may also contribute to vascular injury. C, In chronic rejection with graft arteriosclerosis, injury to the vessel wall leads to intimal smooth muscle cell proliferation and luminal occlusion. This lesion may be caused by a chronic DTH reaction to alloantigens in the vessel wall.

Vascular smooth muscle cell

'Qa-Cytokines

Alloantigen-specific CD4+ T cell

FIGURE 16-8 Immune mechanisms of graft rejection. A, In hyperacute rejection, preformed antibodies reactive with vascular endothelium activate complement and trigger rapid intravascular thrombosis and necrosis of the vessel wall. B, In acute rejection, CD8+ T lymphocytes reactive with alloantigens on endothelial cells and parenchymal cells mediate damage to these cell types. Alloreactive antibodies formed after engraftment may also contribute to vascular injury. C, In chronic rejection with graft arteriosclerosis, injury to the vessel wall leads to intimal smooth muscle cell proliferation and luminal occlusion. This lesion may be caused by a chronic DTH reaction to alloantigens in the vessel wall.

FIGURE 16-9 Histopathology of different forms of graft rejection. A, Hyperacute rejection of a kidney allograft with endothelial damage, platelet and thrombin thrombi, and early neutrophil infiltration in a glomerulus. B, Acute rejection of a kidney with inflammatory cells in the connective tissue around the tubules and between epithelial cells of the tubules. C, Acute antibody-mediated rejection of a kidney allograft with destructive inflammatory reaction destroying the endothelial layer of an artery. D, Complement C4d deposition in vessels in acute antibody-mediated rejection. E, Chronic rejection in a kidney allograft with graft arteriosclerosis. The vascular lumen is replaced by an accumulation of smooth muscle cells and connective tissue in the vessel intima. (Courtesy of Dr. Helmut Rennke, Department of Pathology, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts.)

FIGURE 16-9 Histopathology of different forms of graft rejection. A, Hyperacute rejection of a kidney allograft with endothelial damage, platelet and thrombin thrombi, and early neutrophil infiltration in a glomerulus. B, Acute rejection of a kidney with inflammatory cells in the connective tissue around the tubules and between epithelial cells of the tubules. C, Acute antibody-mediated rejection of a kidney allograft with destructive inflammatory reaction destroying the endothelial layer of an artery. D, Complement C4d deposition in vessels in acute antibody-mediated rejection. E, Chronic rejection in a kidney allograft with graft arteriosclerosis. The vascular lumen is replaced by an accumulation of smooth muscle cells and connective tissue in the vessel intima. (Courtesy of Dr. Helmut Rennke, Department of Pathology, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts.)

humoral, mediated by antibodies, both typically coexist in an acutely rejecting organ.

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