T cell subsets in H. pylori-associated gastritis

摘要: The pathogenesis of chronic gastritis and the presumed causative role Helicobacter pylori has led to considerable dispute in this field research. However, a large number studies involving self-inoculations1,2, epidemiological assessments3,4, histopathological evaluations5–7 fact that after eradication H. marked inflammatory lesions gastric mucosa disappear8,9 have provided compelling evidence suggesting as principal agent form gastritis. Furthermore, therapeutic trials showed combined antibiotic antacid therapy was more effective preventing disease relapse than alone10. Mechanisms involved development mucosal include variety toxins11–14 enzymes secreted by destroy epithelial cells digest protective mucus14,15. Moreover, are characterized lymphocytic infiltrate, specific immune reaction may lead pathology5,6,9. Specifically, it been claimed CD4+ T γδ play critical pylori-associated gastritis16. presence implicated endogenous bacterial heat-shock proteins potential target antigens for local reaction, some investigators reported selectively stimulate vitro 17. Heat-shock group believed function chaperones all prokaryotic eukaryotic expressed at enhanced levels under conditions such physical, thermal or chemical stress order prevent denaturation vital cell function18–20. Importantly, protein expression observed tissues stressed infection19 rheumatoid arthritis conjunction with accumulation cells17. whether pylori-affected represents phenomenon is unclear present, since date not evaluated other forms associated pylori. In addition infiltration within exhibit an increased MHC class II molecules21–23. Therefore, our study we comparatively analysed receptor usage infiltrating lymphocytes regard absence addition, functional status assessed determining IL-2 receptors molecules.