Volpes R, van den Oord J J, Desmet V J
Department of Pathology, University Hospital St. Rafaël, Catholic University of Leuven, Belgium.
Hepatology. 1990 Jul;12(1):59-65. doi: 10.1002/hep.1840120110.
Using monoclonal antibodies and in situ immunohistochemistry, we studied the distribution of "accessory" adhesion molecules (i.e., intercellular adhesion molecule-1 and leukocyte function-associated antigen-3) in 114 liver biopsy specimens with various inflammatory liver diseases and in 12 control liver biopsy samples without inflammation. The distribution of these adhesion molecules was compared with the presence on inflammatory cells of their natural ligands, lymphocyte function-associated antigen-1 and cluster of differentiation antigen-2, respectively. In normal liver, intercellular adhesion molecule-1 and leukocyte function-associated antigen-3 reacted weakly with sinusoidal lining cells, portal vessel endothelium and scattered mononuclear inflammatory cells, whereas hepatocytes were constantly negative. In contrast, all 114 biopsy samples of acute or chronic liver diseases revealed strong expression of intercellular adhesion molecule-1 and leukocyte function-associated antigen-3 on sinusoidal lining cells and on hepatocytes in areas of inflammation. Hepatocellular membrane positivity resulted in a "honeycomb pattern" of staining , which was panacinar in acute hepatitis and focal in chronic persistent or aggressive hepatitis. In various other chronic liver diseases, a multifocal periportal and intraacinar honeycomb pattern was detected. In all cases, a close topographical correlation was found between hepatocellular expression of intercellular adhesion molecule-1 and leukocyte function-associated antigen-3 on one hand and the presence of inflammatory cells expressing lymphocyte function-associated antigen-1 and cluster of differentiation antigen-2 on the other.(ABSTRACT TRUNCATED AT 250 WORDS)
