title: Circulating T-cell response to Helicobacter pylori infection in chronic gastritis.
abstract: BACKGROUND
  Helicobacter pylori elicits a specific humoral and cellular immune response. There is increasing evidence that the type of T-cell response contributes to clinical outcome in H. pylori infection.
  
  
  METHODS
  The host response to H. pylori infection in 34 subjects with chronic gastritis was examined in terms of T-cell proliferation and cytokine production in whole-blood cultures stimulated or unstimulated with H. pylori acid-glycine extract antigens (AGE).
  
  
  RESULTS
  The proliferative response in whole-blood cultures was similar for both H. pylori-positive and -negative subjects stimulated with H. pylori AGE. While an increase in interferon-gamma (IFN-gamma) production was observed from both H. pylori-positive and -negative subjects with gastritis, significantly higher levels of IFN-gamma were detected in the former when stimulated with H. pylori AGE. In contrast, interleukin 4 (IL-4) was undetectable regardless of antigen stimulation. However, if an in situ IL-4 antibody capture assay was used, antigen-independent production of IL-4 was detected, but there was no difference between H. pylori-positive and -negative subjects with gastritis. After eradication of H. pylori, antigen-induced production of IL-4 was increased, with no decrease in the levels of secretion of IFN-gamma. IL-4 production was dependent on CD4+ T cells, as addition of anti-CD4 but not anti-CD8 mouse monoclonal antibody or matched IgG isotype to the whole-blood culture inhibited the production of IL-4.
  
  
  CONCLUSIONS
  The results suggest that a shift toward a balanced Th1-Th2 response due to an increase in antigen-induced IL-4 production from CD4+ T cells follows eradication. We suggest that the downregulation of mucosal inflammation consequent on reduction in antigen levels or removal of downregulation after eradication of H. pylori contributes to this shift in cytokine balance.
authors.affiliation: Discipline of Immunology and Microbiology, Faculty of Medicine and Health Sciences, University of Newcastle, New South Wales, Australia.
authors.forename: Z
authors.initials: Z
authors.lastname: Ren
authors.forename: G
authors.initials: G
authors.lastname: Pang
authors.forename: R
authors.initials: R
authors.lastname: Lee
authors.forename: R
authors.initials: R
authors.lastname: Batey
authors.forename: M
authors.initials: M
authors.lastname: Dunkley
authors.forename: T
authors.initials: T
authors.lastname: Borody
authors.forename: R
authors.initials: R
authors.lastname: Clancy
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000818:Animals; D000900:Anti-Bacterial Agents / Q000627:therapeutic use; D000911:Antibodies, Monoclonal / Q000494:pharmacology; D000942:Antigens, Bacterial / Q000494:pharmacology; D001773:Blood Cells / Q000276:immunology; D015704:CD4 Antigens / Q000276:immunology; D002455:Cell Division / Q000502:physiology; D002478:Cells, Cultured; D005260:Female; D005753:Gastric Mucosa / Q000276:immunology; D005756:Gastritis / Q000276:immunology* / Q000382:microbiology*; D016481:Helicobacter Infections / Q000188:drug therapy / Q000276:immunology*; D016480:Helicobacter pylori; D006801:Humans; D007371:Interferon-gamma / Q000378:metabolism; D015847:Interleukin-4 / Q000378:metabolism; D008297:Male; D051379:Mice; D008875:Middle Aged; D013601:T-Lymphocytes / Q000187:drug effects / Q000276:immunology* / Q000378:metabolism
chemical_list: D000900:Anti-Bacterial Agents; D000911:Antibodies, Monoclonal; D000942:Antigens, Bacterial; D015704:CD4 Antigens; D015847:Interleukin-4; D007371:Interferon-gamma