Chronic infection with hepatitis B virus is widespread, and there are other forms of chronic hepatitis in which the host's immune response is pathogenic. A conference study group report assessed faulty immune effector mechanisms. The immune pathways considered were effector cell recruitment and cytolytic mechanisms, including hepatocyte killing by antigen-specific T lymphocytes, non-antigen-specific cells (K and NK cells, macrophages), and antibody plus complement. Also considered were "modulating" effects of surface-located antibody which could result in reduction of killing by T cells of virus-infected hepatocytes which could facilitate chronicity. Evidence for participation of these immune effector processes has not yet been convincing in human chronic hepatitis. Future research must be directed to defining the type and specificity of cytolytic effector systems and circumstances under which host antibody diminishes or augments the activity of such systems, delineating putative auto-antigens, and developing suitable animals models.