title: Immune phenotype of children with newly diagnosed and gluten-free diet-treated celiac disease.
abstract: BACKGROUND
  Recent data suggest the involvement of both the adaptive and the innate immune system in celiac disease (CD). However, little is known about the immune phenotype of children with CD and its alteration upon dietary intervention.
  
  
  OBJECTIVE
  We characterized the prevalence of major interacting members of the adaptive and innate immune system in peripheral blood of newly diagnosed children with CD and tested its alteration with the improvement of clinical signs after the introduction of gluten-free diet (GFD).
  
  
  METHODS
  Peripheral blood was taken from ten children with biopsy-proven CD at the time of diagnosis and after the resolution of clinical symptoms following GFD. As controls, 15 children with functional abdominal pain were enrolled. The prevalence of the cells of adaptive and innate immunity was measured with labeled antibodies against surface markers and intracellular FoxP3 using a flow cytometer.
  
  
  RESULTS
  Patients with CD were found to have lower T helper, Th1 and natural killer (NK), NKT and invariant NKT cell prevalence and with higher prevalence of activated CD4(+) cells, myeloid dendritic cells (DC) and Toll-like receptor (TLR) 2 and TLR-4 positive DCs and monocytes compared to controls. After resolution of symptoms on GFD, the majority of these changes normalized, although the prevalence of NK and NKT cell, DC and TLR-2 expressing DCs and monocytes remained abnormal.
  
  
  CONCLUSIONS
  The immune phenotype in childhood CD indicates the implication of both adaptive and innate immune system. The normalization of immune abnormalities occurs on GFD, but the kinetics of this process probably differs among different cell types.
authors.affiliation: Research Group for Pediatrics and Nephrology, Semmelweis University and Hungarian Academy of Sciences, First Department of Pediatrics, Bókay u. 53, 1083, Budapest, Hungary. cseharon@gmail.com
authors.forename: Áron
authors.initials: Á
authors.lastname: Cseh
authors.forename: Barna
authors.initials: B
authors.lastname: Vásárhelyi
authors.forename: Balázs
authors.initials: B
authors.lastname: Szalay
authors.forename: Kriszta
authors.initials: K
authors.lastname: Molnár
authors.forename: Dorottya
authors.initials: D
authors.lastname: Nagy-Szakál
authors.forename: András
authors.initials: A
authors.lastname: Treszl
authors.forename: Ádám
authors.initials: Á
authors.lastname: Vannay
authors.forename: András
authors.initials: A
authors.lastname: Arató
authors.forename: Tivadar
authors.initials: T
authors.lastname: Tulassay
authors.forename: Gábor
authors.initials: G
authors.lastname: Veres
mesh_terms: D056704:Adaptive Immunity; D018791:CD4 Lymphocyte Count; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology; D002446:Celiac Disease / Q000175:diagnosis / Q000178:diet therapy* / Q000276:immunology*; D002675:Child, Preschool; D003713:Dendritic Cells / Q000276:immunology; D055050:Diet, Gluten-Free; D005260:Female; D051858:Forkhead Transcription Factors / Q000378:metabolism; D005983:Glutens / Q000009:adverse effects / Q000276:immunology; D006801:Humans; D007113:Immunity, Innate; D007694:Killer Cells, Natural / Q000276:immunology; D008297:Male; D009000:Monocytes / Q000276:immunology; D055611:Natural Killer T-Cells / Q000276:immunology; D010641:Phenotype; D010865:Pilot Projects; D006377:T-Lymphocytes, Helper-Inducer / Q000276:immunology; D018417:Th1 Cells / Q000276:immunology; D051195:Toll-Like Receptor 2 / Q000276:immunology; D051197:Toll-Like Receptor 4 / Q000276:immunology
chemical_list: C418974:FOXP3 protein, human; D051858:Forkhead Transcription Factors; C495342:TLR2 protein, human; C495345:TLR4 protein, human; D051195:Toll-Like Receptor 2; D051197:Toll-Like Receptor 4; D005983:Glutens