The year 1993 was no exception to earlier years, with the publication of new data on the humoral immune response to Helicobacter pylori. Of interest from a fundamental point of view was the observation of mucosal immunoglobulin A autoantibodies to interleukin-8 in chronic gastritis, which may play a role in the down-regulation of inflammation. Three different phagocyte chemotactant components in H. pylori have been described. An increasing amount of data confirms that the major killing effect of H. pylori in vitro is mediated by complement, and is independent of specific antibodies. The variation between strains in producing an oxidative burst in neutrophils, and the increased ability of strains from patients with peptic ulcer disease to induce neutrophil activation, may be of pathogenic importance. The capacity of H. pylori to stimulate natural killer cells and gamma-interferon secretion may also be important.