Abstract
Several lines of evidence implicate Helicobacter pylori (H. pylori) infection in gastroduodenal inflammation. However, the exact pathogenesis of H. pylori infection is not fully understood. T-helper (TH) lymphocytes may be subdivided into TH1 and TH2 cells based on the distinct patterns of cytokine production. TH1 reaction is associated with immunity or resistance to infection, while TH2 reaction is associated with the progression or persistence of infection. The production of interferon-gamma (INF-gamma) and interleukin 2 (IL-2), which are type 1 cytokines, is decreased in H. pylori infection. Enhanced production of type 2 cytokines (IL-4) and IL-6) is observed in individuals with H. pylori infection. Suppressed proliferative responses of peripheral blood and gastric lymphocytes have also been demonstrated in patients with H. pylori colonisation, suggesting that specific T-cell responses may be down-regulated by an enhanced TH2 reaction. Suppressed TH1 and enhanced TH2 responses in H. pylori infection may be involved in the immunopathogenesis of chronic H. pylori infection.
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