Mucosal Immune Regulation and Vaccines for Helicobacter-associated Gastritis

Helicobacter pylori (H. pylori) infects the stomach of more than 50% of humans and causes chronic gastritis in most infected individuals. H. pylori has developed mechanisms to survive the harsh gastric environment. In the host infected with H. pylori, various immune cells infiltrate into the infected gastric mucosa and then severe inflammatory responses occur. This severe inflammation, however, is not able to clear H. pylori and the process may contribute to the associated disease pathogenesis. Toll-like receptor 2 (TLR2) and Nucleotide-binding oligomerization domain-containing protein 1 (NOD1) might be essential for activation of innate immunity against H. pylori infections. Type 1 helper T cells and regulatory T cells induced in stomach and Peyer's patches play an important role in the associated chronic inflammation. Recently, vaccines targeting various factors associated with H. pylori infection have been developed. This review provides information on the mechanisms of the host immune system response against H. pylori infections and the characteristics of H. pylori that enable it to evade host defenses.