Purpose of review. Helicobacter pylorras a.Gram-negative spiral bacterium that colonizes the stomack of humans, causing gastritis, peptic ulcer disease or gastric cancer. H, pylorrinfection accounts for high percentage of mortality and morbidity rates in developing as well as developed countries. H. pylori bacteria reside in the mucus layer covering the gastric epithelium and therefore the type of protective measures that could confer resistance appear to be limited. Although H. pylori infection stimulates strong local and systemic specific IgA and IgG antibody production, the influence of antibodies on bacterial colonization anbd gastric inflammation is still controversial. Recent findings Recent studies in experimental animal models have indicated a non essential role of specific antibodies for host resistance against H. pylori infection. Recent data show that protection is mediated by T cells, CD4 T helper type 1 cells in particular. Antibodies are not only dispensible bor protection , but they impair both the elimination of bacteria and the development of gastritis. This effect appoears to be IgA dependent and is not a function of specific IgM or IgG antibodies. Summary This review highlights the recent advances in our understanding of how antibodies may influence the development of gastric inflammation and bacterial colonization. Such information can significantly increase our basic knowledge of immune regulation and protection against H. pylori infection, but can also indicate new strategies for bvaccine development.