title: Helicobacter pylori has stimulatory effects on naive T cells.
abstract: BACKGROUND
  Despite an apparently active host response, Helicobacter pylori infection can persist for life. Unexpectedly, T cells from apparently uninfected individuals respond to H. pylori antigen by proliferating. Also, the T-cell proliferative response appears to be less in infected compared with uninfected individuals.
  
  
  METHODS
  We have investigated the T-cell response of isolated human peripheral blood, naive, and memory CD4+ T cells to H. pylori antigen in infected and uninfected subjects.
  
  
  RESULTS
  In agreement with previous findings, the peripheral blood proliferative response was higher in uninfected compared with infected subjects. Interestingly, there was a response in CD4+ CD45RO+ (memory) and CD4+CD45RA+ (naive) subsets. The RO/RA ratio of the response to H. pylori antigen was 0.8-2.1 in both H. pylori-positive and H. pylori-negative subjects, which was similar to that of a known superantigen (2.5 and 2.2 in Helicobacter-positive and -negative subjects, respectively) whereas the RO/RA response ratio to a recall antigen (tetanus toxoid) was 9.8 and 18.7 in Helicobacter-positive and -negative subjects, respectively. Mononuclear cells isolated from cord blood also responded to H. pylori antigen, whereas there was no response to tetanus toxoid. The cord blood response and CD4+ CD45RA+ cell response to H. pylori antigen were inhibited predominantly by anti-HLA-DR and to some extent by anti-HLA-DQ antibodies. Investigation of the response to five different recombinant H. pylori antigens identified two that produced a response in naive T cells.
  
  
  CONCLUSIONS
  These data suggest that H. pylori possesses molecules that cause higher than expected proliferation of naive T cells.
authors.affiliation: Department of Infectious Diseases and Microbiology, Hammersmith Campus, Imperial College London, London, UK.
authors.forename: Anna Maria
authors.initials: AM
authors.lastname: Malfitano
authors.forename: Rachel
authors.initials: R
authors.lastname: Cahill
authors.forename: Peter
authors.initials: P
authors.lastname: Mitchell
authors.forename: Gad
authors.initials: G
authors.lastname: Frankel
authors.forename: Gordon
authors.initials: G
authors.lastname: Dougan
authors.forename: Maurizio
authors.initials: M
authors.lastname: Bifulco
authors.forename: Giovanna
authors.initials: G
authors.lastname: Lombardi
authors.forename: Robert I
authors.initials: RI
authors.lastname: Lechler
authors.forename: Kathleen B
authors.initials: KB
authors.lastname: Bamford
mesh_terms: D000911:Antibodies, Monoclonal / Q000494:pharmacology; D000942:Antigens, Bacterial / Q000235:genetics / Q000494:pharmacology; D001426:Bacterial Proteins / Q000235:genetics / Q000494:pharmacology; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology / Q000382:microbiology; D049109:Cell Proliferation; D002478:Cells, Cultured; D006682:HLA-DP Antigens / Q000276:immunology; D006683:HLA-DQ Antigens / Q000276:immunology; D006684:HLA-DR Antigens / Q000276:immunology; D016480:Helicobacter pylori / Q000472:pathogenicity*; D006801:Humans; D007156:Immunologic Memory; D017493:Leukocyte Common Antigens / Q000276:immunology; D011994:Recombinant Proteins / Q000494:pharmacology; D013601:T-Lymphocytes / Q000187:drug effects / Q000276:immunology* / Q000382:microbiology*
chemical_list: D000911:Antibodies, Monoclonal; D000942:Antigens, Bacterial; D001426:Bacterial Proteins; D006682:HLA-DP Antigens; D006683:HLA-DQ Antigens; D006684:HLA-DR Antigens; D011994:Recombinant Proteins; C080866:cagA protein, Helicobacter pylori; D017493:Leukocyte Common Antigens