Helicobacter pylori: Immune Responses and Gastric Autoimmunity

Helicobacter pylori infects almost half of the population worldwide. H. pylori induces the activation of a fascinating cytokine and chemokine network in the gastric mucosa. Chronic H. pylori infection represents a very interesting model of how a single bacterial infection might result in a variety of different clinical outcomes such as duodenal and gastric ulcers, gastric adenocarcinoma, autoimmune gastritis and B cell lymphoma of mucosa-associated lymphoid tissue. The type of host immune response against H. pylori, particularly the cytolytic effector functions of T cells, is crucial for the outcome of the infection. T cells are potentially able to kill a target via different mechanisms, such as perforins or Fas-Fas ligand interaction. In H. pylori-infected patients with gastric autoimmunity, cytolytic T cells that cross-recognize different epitopes of H. pylori proteins and H(+)K(+)-ATPase autoantigen infiltrate the gastric mucosa and lead to gastric atrophy via long-lasting activation of Fas ligand-mediated apoptosis and perforin-induced cytotoxicity. This chapter will focus on the innate immune responses and the role of H. pylori, T cells and cytokines in the onset of autoimmune gastritis.