title: Differences in peripheral blood lymphocyte phenotypes between Helicobacter pylori-positive children and adults with duodenal ulcer.
abstract: The immunological mechanisms involved in the development of duodenal ulcer, especially in childhood, are unclear. Helicobacter pylori-positive children and adults, with and without duodenal ulcer, were therefore compared with respect to CD4(+) T-cells, and CD8(+) T-cells, B-cells and B1a-cells, as well as cell activation (CD4(+)/HLA-DR(+) and CD8(+)/HLA-DR(+)) and co-stimulatory (CD4(+)/CD28(+) and CD8(+)/CD28(+)) markers, in peripheral blood. Children with and without duodenal ulcer differed significantly. In particular, there was a phenotypic change in CD8(+) T-cells from children with ulcer that involved a 200% increase in the number of CD8(+)/HLA-DR(+) cells/mm(3) and a decrease of 34.2% in the number of CD8(+)/CD28(+) cells/mm(3). This phenotype of chronically activated memory CD8(+) T-cells, which has also been observed in patients with AIDS and tuberculosis, is associated with disease severity and progression. A lower frequency of B1a-cells was also observed in the group of children with ulcer. Conversely, no difference between infected adults with and without ulcer was observed, but the percentage of CD4(+)/HLA-DR(+) cells was lower in adults with ulcer, suggesting that a down-regulated immune response may play a role in the development of duodenal ulcer in adults. Gastric inflammation correlated positively with CD4(+) and chronically activated CD4(+) T-cells in children and adults without duodenal ulcer, respectively. These results suggest that there are differences in the immunophenotyping profile between H. pylori-positive children and adults with duodenal ulcer, indicating the possibility of distinct immune mechanisms in the development of the disease according to age.
authors.affiliation: Laboratory of Research in Bacteriology, Faculdade de Medicina/UFMG, Belo Horizonte, Brazil.
authors.forename: T
authors.initials: T
authors.lastname: Figueiredo Soares
authors.forename: G
authors.initials: G
authors.lastname: Aguiar Rocha
authors.forename: A M
authors.initials: AM
authors.lastname: Camargos Rocha
authors.forename: R
authors.initials: R
authors.lastname: Corrêa-Oliveira
authors.forename: O A
authors.initials: OA
authors.lastname: Martins-Filho
authors.forename: A S
authors.initials: AS
authors.lastname: Teles Carvalho
authors.forename: P F
authors.initials: PF
authors.lastname: Souto Bittencourt
authors.forename: C
authors.initials: C
authors.lastname: Afonso Oliveira
authors.forename: A M M
authors.initials: AM
authors.lastname: Ferreira Nogueira
authors.forename: M M D
authors.initials: MM
authors.lastname: Alvares Cabral
authors.forename: A M
authors.initials: AM
authors.lastname: Caetano Faria
authors.forename: D M M
authors.initials: DM
authors.lastname: Queiroz
mesh_terms: D000293:Adolescent; D000328:Adult; D000367:Age Factors; D000368:Aged; D001402:B-Lymphocytes / Q000276:immunology; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology*; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology*; D002648:Child; D004381:Duodenal Ulcer / Q000097:blood / Q000276:immunology*; D005260:Female; D006684:HLA-DR Antigens / Q000276:immunology; D016481:Helicobacter Infections / Q000276:immunology* / Q000382:microbiology; D016480:Helicobacter pylori / Q000276:immunology*; D006801:Humans; D016130:Immunophenotyping / Q000379:methods; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D016176:T-Lymphocyte Subsets / Q000276:immunology
chemical_list: D006684:HLA-DR Antigens