The 60 kDa heat shock proteins (HSP 60) have been well conserved throughout evolution and are highly immunogenic. Cross-reactivity between bacterial and mammalian HSP 60 is considered a likely mechanism in the pathogenesis of autoimmune diseases. T cell and B cell reactivity to HSP 60 is found in patients with rheumatoid or juvenile arthritis, and the expression of HSP 60 in the inflamed joint is found to be increased. In this study the presence of HSP 60 was demonstrated in normal and inflamed lives. HSP 60 was found to be predominantly expressed in hepatocytes and Kupffer cells, and mainly localized in mitochondria. Heat stress in the form of a 1 h incubation at 42 degrees C increased HSP 60 expression. The expression of HSP 60 in chronic active hepatitis was found to be markedly increased, with predominant expression in areas of inflammatory infiltrates. This increased expression in the inflamed liver was found both in viral and autoimmune hepatitis. High expression of HSP 60 in chronic active hepatitis was entirely due to self (i.e. human) HSP 60; no additional bacterial HSP 60 could be detected. Increased expression of HSP 60 in chronic active hepatitis suggests that immune reactions to HSP 60 may play a role in the immunopathogenesis and perpetuation of chronic inflammatory liver disease.