Circulating T-cell response to Helicobacter pylori infection in chronic gastritis

Background. Helicobacter pylori elicits a specific humoral and cellular imm une response. There is increasing evidence that the type of T-cell response contributes to clinical outcome in H. pylori infection. Materials and Methods. The host response to H. pylori infection in 34 subje cts with chronic gastritis was examined in terms of T-cell proliferation an d cytokine production in whole-blood cultures stimulated or unstimulated wi th 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 A GE. While an increase in interferon-gamma (IFN-gamma) production was observ ed from both H. pylori-positive and -negative subjects with gastritis, sign ificantly higher levels of IFN-gamma were detected in the former when stimu lated with H. pylori AGE. In contrast, interleukin 4 (IL-4) was undetectabl e regardless of antigen stimulation. However, if an in situ IL-4 antibody c apture assay was used, antigen-independent production of IL-4 was detected, but there was no difference between H. pylori-positive and -negative subje cts with gastritis. After eradication of H. pylori, antigen-induced product ion of IL-4 was increased, with no decrease in the levels of secretion of I FN-gamma. IL-4 production was dependent on CD4+ T cells, as addition of ant i-CD4 but not anti-CD8 mouse monoclonal antibody or matched IgG isotype to the whole-blood culture inhibited the production of IL-4. Conclusion. The results suggest that a shift toward a balanced Th1-Th2 resp onse due to an increase in antigen-induced IL-4 production from CD4+ T cell s follows eradication. We suggest that the downregulation of mucosal inflam mation consequent on reduction in antigen levels or removal of downregulati on after eradication of H. pylori contributes to this shift in cytokine bal ance.