HISTOPATHOLOGY OF PRIMARY BILIARY-CIRRHOSIS WITH EMPHASIS ON EXPRESSION OF ADHESION MOLECULES

In the initiation and progression of immune-mediated destruction of in terlobular bile ducts and hepatocytes in primary biliary cirrhosis, T- cell-mediated responses to target antigen(s) expressed on the bile duc ts and hepatocytes, as well as cellular adhesions via various adhesion molecules are critical. Intercellular adhesion molecule 1 and, to a l esser degree, vascular adhesion molecule 1 are increasingly expressed on the damaged bile ducts in primary biliary cirrhosis. In addition, l ymphocyte function-associated antigens, very late antigens, endothelia l-leukocyte adhesion molecule I, and other adhesion molecules on the v ascular endothelial cells and/or inflammatory cells, particularly acti vated lymphocytes, are also expressed in the portal tracts and hepatic parenchyma. These adhesion molecules are involved in the extravasatio n as well as epitheliotropic processes of inflammatory cells. Dendriti c cells, particularly interdigitating ones in the periductal tissue, a re positive for these immune molecules and also for the B-7 family. Th ey may also be important in antigen presentation to CD4+ helper T cell s and their activation. However; there is still controversy about whet her the B-7 family is expressed on the bile ducts and, then, whether b iliary epithelial cells work as an antigen presenting cell. Expression of a very late antigen family on the basolateral surface of bile duct s may be involved in the cell-cell and cell-matrix interactions. Solub le adhesion molecules may be involved in the regulation of immune-medi ated bile duct lesions.