Abstract
Background: the neoplastic B cells of the Helicobacter pylori-related low-grade gastric mucosa-associated lymphoid tissue (MALT) lymphoma proliferate in response to H. pylori, however, the nature of the H. pylori antigen responsible for proliferation is still unknown. The purpose of the study was to dissect whether CagY might be the H. pylori antigen able to drive B cell proliferation. Methods: the B cells and the clonal progeny of T cells from the gastric mucosa of five patients with MALT lymphoma were compared with those of T cell clones obtained from five H. pylori–infected patients with chronic gastritis. The T cell clones were assessed for their specificity to H. pylori CagY, cytokine profile and helper function for B cell proliferation. Results: 22 of 158 CD4+ (13.9%) gastric clones from MALT lymphoma and three of 179 CD4+ (1.7%) clones from chronic gastritis recognized CagY. CagY predominantly drives Interferon-gamma (IFN-γ) and Interleukin-17 (IL-17) secretion by gastric CD4+ T cells from H. pylori-infected patients with low-grade gastric MALT lymphoma. All MALT lymphoma-derived clones dose dependently increased their B cell help, whereas clones from chronic gastritis lost helper activity at T-to-B-cell ratios greater than 1. Conclusion: the results obtained indicate that CagY drives both B cell proliferation and T cell activation in gastric MALT lymphomas.
Highlights
Helicobacter pylori is a spiral-shaped Gram-negative bacterium that chronically infects the stomach of more than 50% of the human population, and is the leading cause of gastric cancer, gastric lymphoma, gastric autoimmunity and peptic ulcer diseases [1,2,3,4,5].A strong association between Helicobacter pylori infection and the development of gastric mucosa-associated lymphoid tissue (MALT) lymphoma has been demonstrated [6,7,8]
To characterize at the clonal level the in vivo activated T cells present in the gastric inflammatory infiltrates of H. pylori-infected patients, two cohorts were collected: five untreated patients with gastric low-grade MALT (MALT) and five patients with H. pyloriinduced uncomplicated chronic gastritis (CG)
The results obtained so far suggest that H. pylori CagY is an important factor involved in the genesis of Th1 and Th17 response in H. pylori-infected patients with gastric MALT
Summary
Helicobacter pylori is a spiral-shaped Gram-negative bacterium that chronically infects the stomach of more than 50% of the human population, and is the leading cause of gastric cancer, gastric lymphoma, gastric autoimmunity and peptic ulcer diseases [1,2,3,4,5]. A strong association between Helicobacter pylori infection and the development of gastric mucosa-associated lymphoid tissue (MALT) lymphoma has been demonstrated [6,7,8]. A prerequisite for lymphomagenesis is the development of secondary inflammatory MALT, which is induced by chronic H. pylori infection [7,8]. Their growth depends on antigen-stimulation by H. pylori-specific T cells [11,12]. An important unanswered question remains the chemical nature of the H. pylori factors responsible for the induction of gastric Th cells which can promote the proliferation of The tumor cells of low-grade gastric MALT lymphoma are memory B lymphocytes that still respond to differentiation signals, such as CD40 costimulation and cytokines produced by antigen-stimulated T helper (Th) cells [9,10]
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