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

Abstract EN

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.