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Helicobacter pylori is the dominant member of the gastric microbiota in over half of the human population of which 5-15% develop gastritis or gastric malignancies. Immune responses to H. pylori are characterized by mixed T helper cell, cytotoxic T cell and NK cell responses. The presence of Tregs is essential for the control of gastritis and together with regulatory CX3CR1+ mononuclear phagocytes and immune-evasion strategies they enable life-long persistence of H. pylori. This H. pylori-induced regulatory environment might contribute to its cross-protective effect in inflammatory bowel disease and obesity. Here we review host-microbe interactions, the development of pro- and anti-inflammatory immune responses and how the latter contribute to H. pylori's role as beneficial member of the gut microbiota. Furthermore, we present the integration of existing and new data into a computational/mathematical model and its use for the investigation of immunological mechanisms underlying initiation, progression and outcomes of H. pylori infection.

Original publication




Journal article


Gut Microbes

Publication Date





3 - 21


IFN-γ, bacterial pathogenesis, commensal, helicobacter pylori, host tolerance, immune evasion, information biology, treg, CX3C Chemokine Receptor 1, Gastric Mucosa, Gastritis, Gastrointestinal Microbiome, Helicobacter Infections, Helicobacter pylori, Host-Pathogen Interactions, Humans, Immune Evasion, Immunity, Mucosal, Receptors, Chemokine, Symbiosis, T-Lymphocytes, Helper-Inducer, T-Lymphocytes, Regulatory