Helicobacter pylori Infection: Regulatory T Cells and Their Participation in the Immune Response

Helicobacter pylori is a Gram-negative bacterium that colonizes the human stomach and affects more than half of the global human population. This microorganism shows variations in its geographical distribution and causes chronic gastritis, peptic ulcer, gastric adenocarcinoma and mucosa-associated lymphoid tissue lymphoma. The development of these clinical entities depends on the bacterial strain and its virulence, the host genetic predisposition, immunological response, concurrent infections and infestations. In the immune response for the eradication of H. pylori different types of cells and mediators are involved. Studies reveal that the bacterial infection predominate the cytokines of Th1 phenotype with secretion of abundant levels of IFN-gamma and IL-2 by mucosal T cells. The inability of patients to clear H. pylori infections is a consequence of active immunosuppression and evasive mechanisms of bacteria. Many immune factors are involved: chronic exposure of the DCs to H. pylori leading to DC exhaustion, influence of regulatory T (Treg) cells through immunosuppressive cytokines, and the mast cells that change the gastric mucosal environments among others. In the current review, the focus is restricted to Tregs and their participation in the anti-bacterial response. These cells are a heterogeneous T-cell subpopulation with biological actions determinants in the pathogenesis of H. pylori infection. Studies have demonstrated that the activation of Treg cells cause down-regulation of adaptive immunity facilitating the persistence of infection by H. pylori. Even, the regulations of the Th17/Treg and Th1/Treg balances are important in the immune response against the pathogen, in the persistent colonization of the bacterium and in the affectation of the gastrointestinal system.