In order to understand the pathogenesis of gastric lymphoma, we investigated the association of H.pylori infection with lymphoid follicular hyperplasia. Eighty-four gastric specimens removed for gastroduodenal ulcer were histologically examined. The distribution and prevalence of H. pylori, neutrophilic and lymphocytic infiltration, mucosal atrophy, intestinal metaplasia, and lymphoid follicles were scored. The lymphoid follicles were more frequently observed in H.pylori positive cases. They indicated a positive correlation with the score of H. pylori. When follicular gastritis (FG) was defined as a case in which the secondary lymphoid follicles (Lf2) numbered two or more per one centimeter of mucosa in the pyloric gland area of the lesser curvature, twenty specimens out of the 84 (24%) fit that definition. All of the FG cases were H.pylori positive, and they displayed high H. pylori scores. It was supposed that most FG cases would ultimately lead to atrophic gastritis, whereas H.pylori would gradationally decrease or disappear in accordance with the aging and progression of intestinal metaplasia. The histological features of the FG cases, however, were similar to the background mucosal state of early-stage MALT-type gastric lymphoma. We may conclude that H. pylori infection is one cause of the FG, which may be a high-risk condition that gives rise to MALT-type gastric lymphoma.