Affiliation:
1. Section Molecular Microbiology, Department of Molecular Cell Biology, VU University, De Boelelaan 1085, 1081 HV, Amsterdam, The Netherlands
2. Department of Internal Medicine, University of Florence, viale Morgagni 85, 50134 Florence, Italy
Abstract
Helicobacter pyloriinfection 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 againstH. 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. InH. pylori-infected patients with gastric autoimmunity cytolytic T cells, that cross-recognize different epitopes ofH. pyloriproteins 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 exhaustiveH. pylori-induced T cell-dependent B-cell activation can support both the onset and the promotion of low-grade B-cell lymphoma.
Subject
Health, Toxicology and Mutagenesis,Genetics,Molecular Biology,Molecular Medicine,General Medicine,Biotechnology
Cited by
43 articles.
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