Using monoclonal antibodies and in e i t u immunohietochemietry, we studied the distribution of "acceswry" adhesion molecules (i.e., intercellular adhesion molecule-1 and leukocyte function-associated antigen-3) in 114 liver biopsy specimens with various inflammatory liver dieeases and in 12 control liver biopsy samples without inflammation. The distribution of these adhdon molecules was compared with the presence on atory cells of their natural ligande, lymphocyte function-associated antigen-l and cluater of Merentiation antigen-2, reepectively.
In normal liver, intercellular adhesion molecule-1 and leukocyte function-associated antigen-3 reacted weakly with sinueoidal 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 diaeams, 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-$ on one hand and the presence of inflammatory cells expressing lymphocyte functionassociated antigen-l and cluster of differentiation antigen-2 on the other.
Theee data suggest that in inflammatory liver diseaeea adhedon between hepatocytes and inflammatory cells is mediated by two different pathwaya of cellular interaction, involving intercellular adhesion m o l d elflymphocyte function-associated antigen-1 and leukocyte function-associated antigen-3/cluster of differ-