title: Impaired T-cell regulation of B-cell growth in Helicobacter pylori--related gastric low-grade MALT lymphoma.
abstract: OBJECTIVE
  Neoplastic B cells of the Helicobacter pylori-related low-grade gastric mucosa-associated lymphoid tissue (MALT) lymphoma are responsive to T helper cells and sensitive to withdrawal of H. pylori-induced T-cell help.
  
  
  METHODS
  The clonal progeny of T cells from the gastric mucosa of 5 patients with MALT lymphoma was compared with that of T-cell clones obtained from 5 H. pylori-infected patients with chronic gastritis.
  
  
  RESULTS
  T-cell clones were assessed for specificity to H. pylori, cytokine profile, help for B-cell proliferation, and perforin- or Fas-mediated cytotoxic regulation of B-cell growth. Twenty-eight of 165 CD4(+) gastric clones from MALT lymphoma and 33 of 178 CD4(+) clones from chronic gastritis recognized H. pylori antigens. Cytokine production was similar in the 2 series of clones. 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 because of concomitant cytolytic killing of B cells. T-cell clones from MALT lymphoma had both reduced perforin-mediated cytotoxicity and poor ability to induce Fas-mediated apoptosis. These defects were limited to gastric T cells.
  
  
  CONCLUSIONS
  H. pylori-induced T cell-dependent B-cell activation and deficient cytotoxic control of B-cell growth may link H. pylori infection, local T-cell response, and genesis of low-grade gastric MALT lymphoma.
authors.affiliation: Department of Internal Medicine, University of Florence, Florence, Italy.
authors.forename: M M
authors.initials: MM
authors.lastname: D'Elios
authors.forename: A
authors.initials: A
authors.lastname: Amedei
authors.forename: M
authors.initials: M
authors.lastname: Manghetti
authors.forename: F
authors.initials: F
authors.lastname: Costa
authors.forename: C T
authors.initials: CT
authors.lastname: Baldari
authors.forename: A S
authors.initials: AS
authors.lastname: Quazi
authors.forename: J L
authors.initials: JL
authors.lastname: Telford
authors.forename: S
authors.initials: S
authors.lastname: Romagnani
authors.forename: G
authors.initials: G
authors.lastname: Del Prete
mesh_terms: D000368:Aged; D000942:Antigens, Bacterial / Q000032:analysis / Q000502:physiology; D001402:B-Lymphocytes / Q000276:immunology / Q000473:pathology*; D002455:Cell Division; D002908:Chronic Disease; D002999:Clone Cells; D016207:Cytokines / Q000378:metabolism; D005260:Female; D005753:Gastric Mucosa / Q000378:metabolism; D005756:Gastritis / Q000276:immunology / Q000382:microbiology; D016481:Helicobacter Infections / Q000150:complications*; D016480:Helicobacter pylori / Q000276:immunology; D006801:Humans; D018442:Lymphoma, B-Cell, Marginal Zone / Q000276:immunology / Q000382:microbiology* / Q000473:pathology; D008297:Male; D008562:Membrane Glycoproteins / Q000502:physiology; D008875:Middle Aged; D054353:Perforin; D052899:Pore Forming Cytotoxic Proteins; D013270:Stomach / Q000473:pathology; D013274:Stomach Neoplasms / Q000276:immunology / Q000382:microbiology* / Q000473:pathology; D013601:T-Lymphocytes / Q000276:immunology / Q000378:metabolism / Q000502:physiology*; D006377:T-Lymphocytes, Helper-Inducer / Q000473:pathology; D019014:fas Receptor / Q000502:physiology
chemical_list: D000942:Antigens, Bacterial; D016207:Cytokines; D008562:Membrane Glycoproteins; D052899:Pore Forming Cytotoxic Proteins; D019014:fas Receptor; D054353:Perforin