Expression from the non-protein-coding microRNA (miRNA) miR-155 as well as the master T cell regulator Foxp3 in human lymphocytes via a cAMP-dependent pathway[38]. Both VacA and GGT from H. pylori may possibly also have an effect on T cell activity in an indirect manner by reprogramming dendritic cells to promote the differentiation of naive T cells into T regulatory (Treg) cells[12]. Treg cell differentiation in response to H. pylori infection calls for the direct interaction of naive T cells with “tolerogenic” dendritic cells which have been exposed to H. pylori, either in the gastric mucosa or in gastric or mesenteric lymph nodes[39,40]. Dendritic cells that have been exposed to H. pylori fail to induce TH1 and TH17 form T cell responses in vitro and in vivo; rather, such dendritic cells preferentially induce the expression on the Treg cell-specific transcription factor FOXP3, the surface marker CD25 and the anti-inflammatory cytokine IL-10 in naive T cells[12]. This action may contribute to gastric persistence and immune tolerance throughout infection, and it may independently potentiate the evasion on the immune response generated by the apoptosis of human monocytes within the presence of H. pylori expressing functional cag pathogenicity island[41]. The immune response evasion may also be as a result of induction of COX-2 in gastric epithelial cells by H. pylori GGT[15], which has been shown to suppress the TH1 polarization of T cell response to H. pylori[42]. The effects of H. pylori GGT on T cell-mediated immunity could represent the biological basis of observations in animal models, showing an important role for GGT in H. pylori colonization[5,6]. Mainly because H. pylori has been classified as a variety carcinogen[1], the inhibition of immune responses triggered by H. pylori GGT may also be an essential factor within the induction of malignant MALT lymphoma and adenocarcinoma of the stomach.Buy5-Bromo-2-(tert-butyl)pyridine The effects of H. pylori GGT on T cell-mediated immunity are summarized in Figure three.CONCLUSIONH. pylori produces a mixture of virulence components that damage the gastric mucosa and subvert the host immune response to let persistent colonization in the difficult environment with the human stomach.1414958-33-0 Purity In this critique, we focussed on H.PMID:23833812 pylori GGT, a bacterial protein that inhibits cell proliferation and induces the apoptosis of gastric epithelial cells by way of unique pathways involving ammonia and ROS production. This action mayWJG|wjgnetJanuary 21, 2014|Volume 20|Situation three|Ricci V et al . H. pylori gamma-glutamyl transpeptidaseNT cell CCP NFAT P Nucleus NFATVacADendritic cellNIL-10 IL-NFAT IL-2 transcriptionM GG1 SGGT N CTreg TH17 cell TH1 cellFOXPIL-10, CD25 IL-17 IFNIL-10 IL-17 IFNFigure three Effects of Helicobacter pylori gamma-glutamyl transpeptidase on T cell-mediated immunity. Helicobacter pylori gamma-glutamyl transpeptidase (GGT) and VacA inhibit T cell proliferation and differentiation to T helper 1 (TH1) and TH17. Additionally they protect against T cell immunity by reprogramming dendritic cells to generate interleukin-10 (IL-10) and IL-18 and market the differentiation of naive T cells into T regulatory (Treg) cells that additional suppress T H1 and TH17 effector functions. FOXP3: Forkhead box P3; NFAT: Nuclear aspect of activated T cells; IFN-: Interferon gamma.contribute to gastric injury during H. pylori infection. Interestingly, H. pylori GGT may also stimulate the expression of antiapoptotic factors and aspects that safeguard against cell damage, for example COX-2 and prostaglandins, EGF-related develop.