| Helicobacter pylori (HP) is aerobe and colonizes in the epithelium of the human stomach. Many studies indicated that HP infection was the main cause of gastritis and peptic ulcer and was related with the development of gastric cancer. Many researchers discovered that Thl cells predominated in immune response of patients with acute infection, chronic gastritis or gastric ulcer associated with HP. To explore the changing regularity of Th cells in the procession from chronic superficial gastritis (CSG) to chronic atrophic gastritis (CAG), intestines metaplasia (IM), atypical hyperplasia (AH), and gastric cancer (GC), our investigation were as follows: ①Collect the whole blood from patients with CSG, CAG, IM, AH, GC, or asymptom carriers (AS). And diagnose HP infection by three methods which were Rapid Urease Test of gastric tissue, Urea [14C] breath test and immunoblotting test, ② Take count of Thl cells, Th2 cells and Treg cells in whole blood by Flow cytometry. ③ Detect the expression of IFN-γ and IL-4 in plasma by ELISA. ④ And detect the relative expression of IFN-γ mRNA and IL-4 mRNA in peripheral blood mononuclear cells by Real-time RT-PCR.From all data, we could see that Thl cells were predominant in immune response of patients during the early HP infection. But Th2 cells increased along with the chronicity, which led to the shift from the polarization of Th1 to the polarization of Th2. Furthermore, the number of Treg cells was negatively correlated with Th1/Th2. Treg cells could inhibit Thl cells and Th2 cells, and perhaps mainly inhibit Thl cells which lead to the shift of Th polarization. Those could be provided as direct clinical evidence to explore the immunopathogenesis of HP infection, especially the chronicity of disease and the occur of cancer. |