With the improved survival achieved in the 1980s it has become apparent that graft rejection is a major problem following liver transplantation . Hyperacute rejection is uncommon, although syndromes of fulminant graft failure due to immunological mechanisms have been described. Acute cellular rejection occurs in approximately 70% of patients and usually responds to high-dose steroids. Between 10 and 15% develop chronic rejection, characterised by a progressive destruction of intrahepatic bile ducts which is irreversible . The principal targets of both acute and chronic liver allograft rejection are intrahepatic bile ducts and endothelium . The increased ability of these cell types to express MHC antigens and adhesion molecules may be responsible for their involvement [2, 3] and may be enhanced by the release of proinflammatory cytokines associated with viral infection, particularly CMV . Although the importance of HLA matching remains unknown patients transplanted with ABO incompatible livers have a higher incidence of graft rejection . Lymphocytes probably instigate rejection but liver damage may result from the recruitment of several effector mechanisms involving the activation of neutrophils, macrophages and B cells as well as cytotoxic T cells . Clinical studies are required to determine the optimum immunosuppressive management of liver transplants and in particular to assess the role of new immunosuppressive agents such as monoclonal antibodies and FK506.