Helicobacter pylori is the dominant member of the gastric microbiota and colonizes the stomach of more than 50% of the human population worldwide (1). H. pylori colonization usually does not cause illness, since 85% of infected people remain asymptomatic throughout life, but infection with strains bearing the cag (cytotoxin-associated gene) pathogenicity island can result in peptic ulcer disease, gastric lymphoma, and gastric adenocarcinoma, the second leading cause of cancer-related deaths, in 15% of infected individuals (2, 3). Conversely, there also is increasing evidence of H. pylori providing protection against esophageal and cardial pathologies (4-7), childhood asthma (8-10), childhood allergies (9, 11), and diabetes and obesity (12). This Gram-negative microaerophilic bacterium of the Epsilonproteobacteria has coevolved with humans for at least 50,000 years, indicating high adaptation capacity to the environmental niche of the human gastric mucosa and suggesting the ability to evade the immune system (13) through mechanisms that are incompletely understood. Infection with H. pylori in humans is associated mainly with a mucosal Th1 response, which is unsuccessful in clearing the bacteria from the stomach and can lead to more severe immunopathology (14). The pathogenicity of H. pylori is determined by various hostand pathogen-related factors, including the host's genetic background, age, and immune status and the bacterium's ability for antigenic variation, molecular mimicry, intracellular persistence, and expression of pathogenicity factors (15).Regulatory T (Treg) cells play a crucial role in H. pylori's ability to evade the immune system and persist in the gastric mucosa. Specifically, H. pylori can trigger a reprogramming of dendritic cells (DC) by downregulating major histocompatibility complex II (MHC-II) and inducing interleukin-10 (IL-10) and inhibiting IL-12 secretion, thereby inducing H. pylori-specific Treg cells (16)(17)(18). B cells also play a regulatory role by promoting IL-10 production in cocultured CD4 ϩ cells and subsequent conversion into a T T lymphocytes were found in the gastric epithelium and lamina propria (LP) of H. pylori-infected children with grade I to III gastritis (22, 23). Furthermore, the CD8 ϩ HLA-DR ϩ chronically activated memory T cell subset was expanded in peripheral blood of H. pylori-colonized children with duodenal ulcers (24), suggesting a role for CD8 ϩ T cells in H. pylori-mediated pathology. The majority of in vivo studies on the host responses to H. pylori are based on mouse models; however, in contrast to human