title: Increase of antigen-presenting cells in the gastric mucosa of Helicobacter pylori-infected children.
abstract: BACKGROUND
  Infection with Helicobacter pylori leads to an increase of T cells in the gastric mucosa of children. In contrast to peripheral blood, where monocytes are the most abundant antigen-presenting cells, CD14+ macrophages are very rare in infected gastric mucosa. We postulated that other types of antigen-presenting cells must be present in infected gastric mucosa.
  
  
  METHODS
  Antral biopsies were obtained from 56 children. The cellular expression of major histocompatibility complex (MHC) class II molecules, CD1a/b, and CD23, which are involved in antigen presentation were analyzed by immunohistochemistry. In addition, T cells (CD4, CD8, CD25, and gamma/delta-TCR), B cells (anti-IgM), macrophages (CD14) and granulocytes (CD15) were quantified.
  
  
  RESULTS
  Twenty-eight children were H. pylori-infected. Thirteen children were healthy, 15 had other gastric pathologies. T cells (p<.0001), B cells (p<.0001), CD23+ (p<.0001), and CD1a/b+ (p<.005) cells were significantly increased in the lamina propria of H. pylori-infected children, whereas macrophages were rare without significant differences among the groups. Within the epithelium, CD8+ T lymphocytes predominated clearly over CD4+ cells. H. pylori-negative children had only few MHC class II-positive cells within the gastric epithelium, whereas MHC class II antigens were strongly expressed on epithelial cells (p<.0001) of all H. pylori-infected children.
  
  
  CONCLUSIONS
  Helicobacter pylori infection leads to an enhanced expression of antigen-presenting molecules together with a parallel rise of T cells in the lamina propria. This may represent an effort of the immune system to optimize local immune responses against H. pylori. We speculate that the epithelium participates in the initiation of a local immune response against H. pylori.
authors.affiliation: Children's Hospital of the Ludwig-Maximilians-University, Munich, Germany. susanne.krauss-etschmann@med.uni-muenchen.de
authors.forename: Susanne
authors.initials: S
authors.lastname: Krauss-Etschmann
authors.forename: Rudolf
authors.initials: R
authors.lastname: Gruber
authors.forename: Katinka
authors.initials: K
authors.lastname: Plikat
authors.forename: Isabel
authors.initials: I
authors.lastname: Antoni
authors.forename: Hans
authors.initials: H
authors.lastname: Demmelmair
authors.forename: Dietrich
authors.initials: D
authors.lastname: Reinhardt
authors.forename: Sibylle
authors.initials: S
authors.lastname: Koletzko
mesh_terms: D000293:Adolescent; D000938:Antigen-Presenting Cells / Q000276:immunology*; D001402:B-Lymphocytes / Q000276:immunology; D002648:Child; D002675:Child, Preschool; D004848:Epithelium / Q000276:immunology / Q000382:microbiology; D005260:Female; D005753:Gastric Mucosa / Q000276:immunology / Q000382:microbiology*; D016481:Helicobacter Infections / Q000276:immunology* / Q000382:microbiology; D016480:Helicobacter pylori / Q000276:immunology* / Q000472:pathogenicity; D000949:Histocompatibility Antigens Class II / Q000378:metabolism; D006801:Humans; D007223:Infant; D008297:Male; D016176:T-Lymphocyte Subsets / Q000276:immunology
chemical_list: D000949:Histocompatibility Antigens Class II