title: Indications for a disturbed peripheral T-cell homeostasis in juvenile idiopathic arthritis (JIA): absent expansion of CD28 T-cells and no decrease of naive T-cells in cytomegalovirus-positive patients with JIA.
abstract: OBJECTIVE
  To investigate the influence of latent cytomegalovirus (CMV) and Epstein-Barr virus (EBV) infections on CD28-expressing T-cell subpopulations and replicative senescence of naive T-cells as a marker for aging of the immune system in children with juvenile ideopathic arthritis (JIA).
  
  
  METHODS
  T-cell subpopulations were analyzed from 24 patients with JIA and 61 healthy age-matched controls by fluorescence activated cell sorting. Relative telomere length (RTL) in CD4+CD28+CD45RA+ (naive) T-cells was measured by quantitative polymerase chain reaction.
  
  
  RESULTS
  Although confirming known data of expansions of CD28- T-cells and tendency of decreasing naive T-cells in CMV-seropositive healthy individuals, our findings did not show a marked influence of latent EBV or CMV infection on CD28-expressing T-cells in patients with JIA. In contrast, CMV was an independent factor for loss of CD28, regardless of age, in healthy controls. Irrespective of serology results for CMV or EBV, patients with JIA showed signficantly decreased RTL compared to age-matched controls. Regression lines for RTL and age revealed decreased RTL with advancing age in CMV-positive and EBV-positive subjects. The evidence that findings for CMV-positive JIA patients did not resemble the findings of healthy CMV-positive controls, namely expansion of CD28- T-cells and decrease of naive T-cells, may support the theory of a disturbed peripheral T-cell homeostasis in JIA.
  
  
  CONCLUSIONS
  Diminished mechanisms of T-cell homeostasis and premature aging of the immune system may play a role in the pathogenesis of JIA.
authors.affiliation: Department of Pediatrics, Medical University Innsbruck, Innsbruck, Austria. Martina.Prelog@i-med.ac.at
authors.forename: Martina
authors.initials: M
authors.lastname: Prelog
authors.forename: Nora
authors.initials: N
authors.lastname: Schwarzenbrunner
authors.forename: Michaela
authors.initials: M
authors.lastname: Sailer-Hoeck
authors.forename: Hannelore
authors.initials: H
authors.lastname: Kern
authors.forename: Christian
authors.initials: C
authors.lastname: Koppelstaetter
authors.forename: Reinhard
authors.initials: R
authors.lastname: Wurzner
authors.forename: Lothar Bernd
authors.initials: LB
authors.lastname: Zimmerhackl
authors.forename: Juergen
authors.initials: J
authors.lastname: Brunner
mesh_terms: D000293:Adolescent; D001171:Arthritis, Juvenile / Q000276:immunology* / Q000503:physiopathology / Q000821:virology*; D018106:CD28 Antigens / Q000276:immunology*; D016022:Case-Control Studies; D002648:Child; D002675:Child, Preschool; D015331:Cohort Studies; D003586:Cytomegalovirus Infections / Q000276:immunology*; D020031:Epstein-Barr Virus Infections / Q000276:immunology; D006706:Homeostasis; D006801:Humans; D016176:T-Lymphocyte Subsets / Q000648:ultrastructure / Q000821:virology*; D016615:Telomere / Q000648:ultrastructure; D017735:Virus Latency / Q000276:immunology
chemical_list: D018106:CD28 Antigens