Abstract
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.
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Neuberger, J., Adams, D., Hubscher, S. (1993). Expression of ICAM-1 in Human Liver. In: Lipsky, P.E., Rothlein, R., Kishimoto, T.K., Faanes, R.B., Smith, C.W. (eds) Structure, Function, and Regulation of Molecules Involved in Leukocyte Adhesion. Springer, New York, NY. https://doi.org/10.1007/978-1-4613-9266-8_30
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DOI: https://doi.org/10.1007/978-1-4613-9266-8_30
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