title: Natural Killer Cell Subsets and IL-2, IL-15, and IL-18 Genes Expressions in Chronic Kidney Allograft Dysfunction and Graft Function in Kidney Allograft Recipients.
abstract: BACKGROUND
  While acute rejection and early graft loss rates have decreased substantially over the past four decades, progressive chronic allograft dysfunction (CAD) still remains a common cause of late graft loss in kidney transplant recipients.
  
  
  OBJECTIVE
  This study was conducted to investigate the percentage of natural killer (NK) cell subsets and IL-2, 15 and 18 genes expression in two groups of CAD and well-function graft (WFG) recipients.
  
  
  METHODS
  30 renal allograft recipients with biopsy-proven interstitial fibrosis/tubular atrophy (IF/TA) and impaired renal function, and 30 sex- and age-matched WFG patients were enrolled in this study. The percentage of NK cell subsets including NK CD56brightand NK CD56dimcells were determined by flowcytometry; IL-2, IL-15, and IL-18 genes expressions were assessed by real-time PCR.
  
  
  RESULTS
  Compared to WFG patients, there was a significant (p<0.05) increase in the percentage of NK CD56brightcells in CAD patients. However, the difference in percentage of NK CD56dimcells or CD56dim/CD56brightratio between the studied groups was not significant. In addition, IL-2, 15 and 18 genes expressions were almost similar in CAD and WFG patients.
  
  
  CONCLUSIONS
  We found higher percentages of NK CD56brightsubset in kidney transplant recipients with CAD without considerable changes in related cytokines' gene expression, suggesting a possible defect of NK cells maturation in these patients.
authors.affiliation: Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
authors.forename: S
authors.initials: S
authors.lastname: Assadiasl
authors.affiliation: Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
authors.forename: A
authors.initials: A
authors.lastname: Sepanjnia
authors.affiliation: Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
authors.forename: B
authors.initials: B
authors.lastname: Aghili
authors.affiliation: Chronic Kidney Disease Research Center, Labbafinejad Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
authors.forename: M
authors.initials: M
authors.lastname: Nafar
authors.affiliation: Chronic Kidney Disease Research Center, Labbafinejad Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
authors.forename: P
authors.initials: P
authors.lastname: Ahmadpoor
authors.affiliation: Chronic Kidney Disease Research Center, Labbafinejad Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
authors.forename: F
authors.initials: F
authors.lastname: Pourrezagholi
authors.affiliation: Department of Pathology, Labbafinejad Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
authors.forename: M
authors.initials: M
authors.lastname: Parvin
authors.affiliation: Molecular Immunology Research Center, Tehran University of Medical Sciences, Tehran, Iran.
authors.forename: A
authors.initials: A
authors.lastname: Shahlaee
authors.affiliation: Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran; Molecular Immunology Research Center, Tehran University of Medical Sciences, Tehran, Iran.
authors.forename: M H
authors.initials: MH
authors.lastname: Nicknam
authors.affiliation: Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran; Molecular Immunology Research Center, Tehran University of Medical Sciences, Tehran, Iran.
authors.forename: A
authors.initials: A
authors.lastname: Amirzargar
keywords: Chronic allograft dysfunction; Interleukin gene expression; Natural killer cells