We investigated the role of the interferon system in the pathogenesis of chronic liver disease. Interferon-? production by peripheral blood mononuclear cells was meaeured with an ELISA. While concanavalin A-stimdated and recombinant interleukin 2-stimulated production of interferon-y in patients with chronic active hepatitis and liver cirrhosis was significantly decreased when compared with that of controls (518 f 189 and 729 f 195 units per ml, mean 2 S.D.), there was also a lot of overlap. Addition of indomethacin to the cultures partially restored interferon-7 production in patients with chronic active hepatitis and liver cirrhosis, indicating that suppressor function of monocytes was, in part, responsible for the diminished interferon-y production. Serial studies showed that interferon-y production rose during acute deterioration of illness, during treatment with interleukin 2 and with the improvement of clinical course. Interferon-7 production was not different among hepatitis B e antigen or antibody positive, and non-A, non-B patients with chronic active hepatitis and liver cirrhosis. Our findings suggest that d i m i e d interferon-y production is associated with disease severity in chronic liver disease, irrespective of the hepatitis B virus carrier state. It would be interesting to compare the efficacy of treatment with interferon-7 or interferon-y inducers such as interleukin 2 in chronic hepatitis B patients with and without decreased in uitro interferon-y production.
Interferons (IFNs) represent a family of proteins with many biological activities. On the basis of different biochemical and immunological properties, IFNs can be placed into three major classes: IFNa, IFNB and IFNr (1, 2). IFNs inhibit the replication of viruses, suppress the proliferation of malignant cells in uitm and exert immunomodulatory activities. Thus, the network of pathways which constitute the IFN system plays an important role in host-defense mechanism against viral infection. IFNr is produced during an immune response by antigen-specific T cells and probably also by natural killer cells recruited by interleukin 2 (IL2) of T cell origin
(3).
Although the factors determining the outcome of hep-