Expression of ICAM-1 in Human Liver
Immune mechanisms are involved in the pathogenesis and progression of liver damage in a number of different disorders. Perhaps the best example of immune mechanisms causing liver damage occurs in allograft rejection. Liver transplantation has now become an accepted form of treatment for end-stage liver disease. As with other organ grafts, rejection remains a significant problem. Overimmunosuppression results in increased susceptibility to infection and underimmunosuppression leads to progressive graft damage due to immune-mediated rejection. Of the different forms of liver allograft rejection, acute rejection is the commonest, occurring in up to 70% of patients (1,2). Over 80% of instances respond to a short course of high-dose corticosteroids. The characteristic histological features of acute allograft rejection include bile duct damage; portal tract inflammation with infiltration by lymphocytes, eosinophils, neutrophils, and monocytes; and venous endotheliales. The other form of rejection is chronic/ductopenic rejection. This occurs in 10% of allograft recipients. Clinically, the onset is usually apparent within the first 6 months after transplantation. In the early stages there is an intense lymphocyte infiltration around the portal tract, but as the disease progresses, the infiltration becomes less.
KeywordsHepatitis Filtration Acetone Ischemia Corticosteroid
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