Lymphocytic gastritis is characterized by the accumulation of small lymphocytes within the surface and foveolar epithelium, however its cause has not been proven. As compared with chronic active gastritis, the local immunoreaction of lymphocytic gastritis was immunohistochemically studied. Although many organisms of Helicobacter pylori (H. pylori) were immunohistochemically detected in all cases with chronic active gastritis, a few organisms were scattered only in 4 cases (28.6%) with lymphocytic gastritis. The extent of HLA-DR-expression in the foveolar epithelium was significantly higher in H. pylori-gastritis than in lymphocytic gastritis, and that of beta 2-microglobulin-expression in the surface epithelium was higher in lymphocytic gastritis than in H. pylori-gastritis. Numerous intraepithelial lymphocytes in lymphocytic gastritis were proved to be CD8-positive cytotoxic/suppressor T-lymphocytes. Our findings suggest that MHC-class I-expression is closely related to the pathogenesis of lymphocytic gastritis. Therefore, some intracellular autoantigens, molecularly mimicking viral antigens, may play a role in its pathogenesis. These autoantigens might occur probably associated not only indirectly with H. pylori-infection but also with unknown viral infection, food intake, bile reflux or stomach tumor.