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lüll Cytotoxic T cells in H pylori-related gastric autoimmunity and gastric lymphoma Bergman MP; D'Elios MMJ Biomed Biotechnol 2010[]; 2010 (ä): 104918Helicobacter pylori infection is the major cause of gastroduodenal pathologies, but only a minority of infected patients develop gastric B-cell lymphoma, gastric autoimmunity, or other life threatening diseases, as gastric cancer or peptic ulcer. The type of host immune response against H. pylori, particularly the cytolytic effector functions of T cells, is crucial for the outcome of the infection. T cells are potentially able to kill a target via different mechanisms, such as perforins or Fas-Fas ligand interaction. In H. pylori-infected patients with gastric autoimmunity cytolytic T cells, that cross-recognize different epitopes of H. pylori proteins and H(+)K(+)-ATPase autoantigen, infiltrate the gastric mucosa and lead to gastric atrophy via long-lasting activation of Fas ligand-mediated appotosis and perforin-induced cytotoxicity. On the other hand, gastric T cells from MALT lymphoma exhibit defective perforin- and Fas-Fas ligand-mediated killing of B cells, with consequent abnormal help for B-cell proliferation, suggesting that deregulated and exhaustive H. pylori-induced T cell-dependent B-cell activation can support both the onset and the promotion of low-grade B-cell lymphoma.|*Autoimmune Diseases[MESH]|*Helicobacter pylori[MESH]|*Lymphoma, B-Cell, Marginal Zone[MESH]|*Stomach Neoplasms[MESH]|*T-Lymphocytes, Cytotoxic[MESH]|Animals[MESH]|Disease Models, Animal[MESH]|Humans[MESH]|Mice[MESH] |