Abstract
Immunologic phenomena as pathogenic principles of chronic liver disease were first suggested by Fiessinger (1) in 1908. In 1950 Waldenstrom (2) described a group of young women with chronic liver disease and marked hypergamma-globulinaemia. During the subsequent years many papers were published about similar patients, mostly with endocrinologic abnormalities such as amenorrhoea or acne. In 1956 Mackay et al. (3) postulated an autoimmune hepatitis based on the detection of antibodies to organ and species non-specific nuclear antigens. They introduced the term ‘lupoid’ hepatitis by analogy with systemic lupus erythematosus; they also proposed a hypothesis involving the expression of forbidden clones of lymphocytes as a means of explaining tissue damage through abrogation of tolerance. In 1963 Blumberg et al. (4) found an antigen associated with serum hepatitis, and it became clear from this finding that chronic hepatitis had a different aetiology.