Immunological aspects of clinical liver transplantation.
With the improved survival achieved in the 1980s it has become apparent that graft rejection is a major problem following liver transplantation [1]. 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 [2]. The principal targets of both acute and chronic liver allograft rejection are intrahepatic bile ducts and endothelium [2]. 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 [3]. Although the importance of HLA matching remains unknown patients transplanted with ABO incompatible livers have a higher incidence of graft rejection [4]. 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 [5]. 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.
Adams
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Liver Unit, Queen Elizabeth Hospital, Birmingham, U.K.
D000017:ABO Blood-Group System / Q000276:immunology; D000208:Acute Disease; D002908:Chronic Disease; D006084:Graft Rejection / Q000187:drug effects / Q000276:immunology; D006680:HLA Antigens / Q000276:immunology; D006801:Humans; D007166:Immunosuppressive Agents / Q000627:therapeutic use; D016031:Liver Transplantation / Q000276:immunology*
D000017:ABO Blood-Group System; D006680:HLA Antigens; D007166:Immunosuppressive Agents