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Journal of Biomedicine and Biotechnology
Volume 2010 (2010), Article ID 104918, 10 pages
Review Article

Cytotoxic T Cells in H. pylori-Related Gastric Autoimmunity and Gastric Lymphoma

1Section Molecular Microbiology, Department of Molecular Cell Biology, VU University, De Boelelaan 1085, 1081 HV, Amsterdam, The Netherlands
2Department of Internal Medicine, University of Florence, viale Morgagni 85, 50134 Florence, Italy

Received 18 January 2010; Accepted 28 April 2010

Academic Editor: Gad Frankel

Copyright © 2010 Mathijs P. Bergman and Mario M. D'Elios. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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 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.