Nr. 2 - 2. Quartal 1994

Distribution of HLA Antigens and Cytokeratin Pattern of Human Gallbladder Epithelial Cells Isolated from Liver Transplant Organs

M. K. H. Auth et al.

Acute or chronic episodes of liver allograft rejection are characterized by the destruction of the biliary epithelium. The diagnosis of an intrahepatic cholestasis and the histopathological observation of bile duct loss is also associated with infections, ischemia, immunologically mediated diseases or it is a side-effect of drug therapy. In order to examine mechanisms of allograft rejection, pathways of infections, and the effect of immunosuppressive drugs, in vitro investigations with human biliary epithelial cells are a practical model. We used human gallbladder epithelial cells because of their availability fom the donor and the recipient liver transplant organ (n=10), and their excellent isolation and culture conditions. In order to examine the relationship of the cells in terms of embryological and immunological features, immunoperoxidase stainings with monoclonal antibodies typical for the intrahepatic biliary epithelium were performed. Stainings directed against cytokeratin numbers 1 through 8, 18, 19 and HEA 125, as well as HLA class I antigens, were always positive. On the contrary, expression of HLA class II antigens was negative (HLA-DP and DQ) or only detectable (HLA-DR). Adhesion molecule ICAM-1 was expressed weakly positive in all cases. Therefore, we were able to show that human gallbladder epithelial cells are very similar to intrahepatic bile duct cells concerning their antigen pattern. The in vitro culture of human gallbladder epithelial cells from the transplant organ may well further allow studies on their recognition by host-lymphocytes leading to bile ductular damage in liver allograft rejection. In addition, the mechanisms of infection, e.g. with cytomegalovirus, and the effect of the immunosuppressive drug therapy may be evaluated.

Keywords:

Liver transplantation, HLA antigens, biliary epithelium, cell culture

Kurztitel:

Auth, M. K. H. (1994) TxMed 2:79

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