Adhesive molecules in liver disease

Abstract

The distribution of the thrombospondin-receptor was studied in 26 cases of inflammatory hepatitis B virus (HBV) related liver disease and twelve non-inflammatory controls using monoclonal antibody (mcab) OKM5. OKM5 reacted in all cases with sinusoidal lining cells, portal vessel endothelium, and scattered mononuclear inflammatory cells. In 16 of the 26 cases with inflammation, one or more clusters of OKM5 positive (OKM5+) hepatocytes were found in areas of periportal or intralobular inflammation, whereas the remaining ten cases did not show hepatocellular OKM5 reactivity. In all but one case, OKM5+ liver cells coexpressed HLA-DR-antigens, and in twelve cases cytotoxic/suppressor T-cells were enriched in the OKM5+/HLA-DR+ liver cell clusters, suggesting induction of OKM5 positivity by lymphokines released by nearby T-cells. In view of its role in cytoadherence, it is suggested that OKM5 expression by hepatocytes serves in the entrapment and retention of inflammatory cells thereby facilitating their activation. Furthermore, OKM5+/HLA-DR+ hepatocytes might trigger an autologous mixed lymphocyte reaction (AMLR), resulting in down-modulation of ongoing hepatic inflammatory responses.