The term of "follicular hapatitis" has been proposed to certain cases of chronic active hepatitis with an intense lymphoid cell accumulation forming a follicular appearance in the portal triads. In this study, the ultrastructural analysis of the lymphoid cells forming a follicular accumulation in the portal tracts, and of a relationship between the mesenchymal cells and hepatocytes at the destructed limiting plate was attempted. Ultrathin sections of the liver biopsy specimens obtained from a patient with follicular hepatitis were cut immediately adjacent to a semithin section which was stained with toluidin blue and in which the follicular accumulation of lymphoid cells and a destructed limiting plate were observed through a light microscope. The center of the follicules consisted of immunoblasts and reticulum cells of both the nonphagocytic branching and phagocytic varieties. Lymphoblasts, immature and numerous mature lymphocytes, plasma cells and a small number of macrophages were observed surrounding the center. The mitotic figure of these mesenchymal cells was found to be on the increase. Macrophages were also found in the area where the liver cells and the portal tracts adjoined. No hepatocellular degeneration was observed at the sharp border between parenchyma and portal tracts. In the area showing the destructed limiting plate, lymphocytes and, occasionally, plasma cells were adjacent to hepatocytes and/or ductular cells. These mesenchymal cells, especially the lymphocytes, indented the hepatocytes and, sometimes, their plasma menbranes were coapted. The hepatocytes lacked microvilli at the area of coaptation, and the degeneration of their cell organelles that was a marked vesiculation and vacuolization of endoplasmic reticulum accompanying a loss of ribosomes, was observed near the coaptation. In the ductular cells coapted with lymphocytes, similar degeneration of the cell organelles was observed and basement membranes disappeared. These results revealed that in these follicules in protal triads mesencymal cells actively responded to antigen stimulation and that a cellular immunity might also be involved in the pathogenesis of chronic active hepatitis.