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- W2080478624 abstract "Helicobacter 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 -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." @default.
- W2080478624 created "2016-06-24" @default.
- W2080478624 creator A5007986321 @default.
- W2080478624 creator A5071144220 @default.
- W2080478624 date "2010-01-01" @default.
- W2080478624 modified "2023-10-15" @default.
- W2080478624 title "Cytotoxic T Cells in<i>H. pylori</i>-Related Gastric Autoimmunity and Gastric Lymphoma" @default.
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