title: Histopathology of primary biliary cirrhosis with emphasis on expression of adhesion molecules.
abstract: In the initiation and progression of immune-mediated destruction of interlobular bile ducts and hepatocytes in primary biliary cirrhosis, T-cell-mediated responses to target antigen(s) expressed on the bile ducts and hepatocytes, as well as cellular adhesions via various adhesion molecules are critical. Intercellular adhesion molecule 1 and, to a lesser degree, vascular adhesion molecule 1 are increasingly expressed on the damaged bile ducts in primary biliary cirrhosis. In addition, lymphocyte function-associated antigens, very late antigens, endothelial-leukocyte adhesion molecule 1, and other adhesion molecules on the vascular endothelial cells and/or inflammatory cells, particularly activated lymphocytes, are also expressed in the portal tracts and hepatic parenchyma. These adhesion molecules are involved in the extravasation as well as epitheliotropic processes of inflammatory cells. Dendritic cells, particularly interdigitating ones in the periductal tissue, are positive for these immune molecules and also for the B-7 family. They may also be important in antigen presentation to CD4+ helper T cells and their activation. However, there is still controversy about whether the B-7 family is expressed on the bile ducts and, then, whether biliary epithelial cells work as an antigen presenting cell. Expression of a very late antigen family on the basolateral surface of bile ducts may be involved in the cell-cell and cell-matrix interactions. Soluble adhesion molecules may be involved in the regulation of immune-mediated bile duct lesions.
authors.affiliation: Second Department of Pathology, Kanazawa University School of Medicine, Japan.
authors.forename: Y
authors.initials: Y
authors.lastname: Nakanuma
authors.forename: M
authors.initials: M
authors.lastname: Yasoshima
authors.forename: K
authors.initials: K
authors.lastname: Tsuneyama
authors.forename: K
authors.initials: K
authors.lastname: Harada
mesh_terms: D017951:Antigen Presentation; D000938:Antigen-Presenting Cells / Q000276:immunology / Q000473:pathology; D001324:Autoantigens / Q000276:immunology; D001327:Autoimmune Diseases / Q000473:pathology*; D018122:B7-1 Antigen / Q000032:analysis / Q000235:genetics; D001653:Bile Ducts, Intrahepatic / Q000276:immunology / Q000473:pathology; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology / Q000473:pathology; D002448:Cell Adhesion; D015815:Cell Adhesion Molecules / Q000032:analysis* / Q000235:genetics; D002450:Cell Communication; D003713:Dendritic Cells / Q000276:immunology / Q000473:pathology; D019040:E-Selectin / Q000032:analysis / Q000235:genetics; D004730:Endothelium, Vascular / Q000276:immunology / Q000473:pathology; D004848:Epithelium / Q000276:immunology / Q000473:pathology; D005109:Extracellular Matrix / Q000276:immunology; D015870:Gene Expression; D006801:Humans; D007249:Inflammation; D018799:Intercellular Adhesion Molecule-1 / Q000032:analysis / Q000235:genetics; D008099:Liver / Q000276:immunology / Q000473:pathology; D008105:Liver Cirrhosis, Biliary / Q000276:immunology / Q000473:pathology*; D008213:Lymphocyte Activation; D016169:Lymphocyte Function-Associated Antigen-1 / Q000032:analysis / Q000235:genetics; D016029:Receptors, Very Late Antigen / Q000032:analysis / Q000235:genetics; D013601:T-Lymphocytes / Q000276:immunology / Q000473:pathology; D006377:T-Lymphocytes, Helper-Inducer / Q000276:immunology / Q000473:pathology; D019010:Vascular Cell Adhesion Molecule-1 / Q000032:analysis / Q000235:genetics
chemical_list: D001324:Autoantigens; D018122:B7-1 Antigen; D015815:Cell Adhesion Molecules; D019040:E-Selectin; D016169:Lymphocyte Function-Associated Antigen-1; D016029:Receptors, Very Late Antigen; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1