Cytokine profile of H. pylori specific T cells differs between peptic ulcer disease and non-ulcer chronic gastritis

The pattern of cytokines secreted by Helicobacter pylori (Hp) specific T cells at gastic level is believed to play a role in the outcome of the infection. To assess the local cellular immune response in H. pylori infection, we analyzes the cytokine profile of specific T-call clones generated from antra/biopsies of 7 Hp infected patients, of which 5 suffered from duodenal ulcer and 2 from non-ulcer gastritis. Twenty-four CD4+ T-cell clones dedved from duodenal ulcer patients proliferates to Hp antigens. Upon stimulation with the specific antigen, 20 of the 24 clones (83%) showed a polarized Th1cytokine profile (i.e. produced IFN-y but not IL-4 nor IL-5), whereas 4 clones were Th0, producing IFN-g,, IL-4 and/or IL-5. In contrast, among the 16 Hp-specific CD4+ T-call clones derived from the antrum of non-ulcer chronic gastritis patients, only 7 (44%) were polarized Th1 and the other 9 (56%) were Th0 effectors. We suggest that H. pylori infection associates with a predominant Th1 response leads to duodenal ulcer through cytokine induced gastric hyperacidity, whereas in non-ulcer chronic gastritis the expression of Th1 cytokines is more frequently balanced by the production of Th2 cytokines, which may exert a protective effect.