title: Invariant natural killer T cells are depleted in renal impairment and recover after kidney transplantation.
abstract: BACKGROUND
  Altered immune function in patients with renal failure results in both susceptibility to infection and increased inflammatory response. Invariant natural killer T (iNKT) cells are a conserved, immunoregulatory T lymphocyte subset that responds to lipid antigens with near-immediate cytokine production and cytotoxicity. iNKT cells are required for the antibacterial host response. Whether renal failure and renal replacement therapy alter iNKT cell abundance or phenotype has not been investigated.
  
  
  METHODS
  iNKT cells were studied by flow cytometry in the peripheral blood of patients with acute renal failure, chronic haemo- and peritoneal dialysis (PD), chronic kidney disease and after renal transplantation.
  
  
  RESULTS
  A very marked reduction in iNKT lymphocytes was found in acute renal failure before the first haemodialysis (HD) session. iNKT cells were depleted in end-stage renal disease patients receiving either HD or PD. iNKT cell depletion was accentuated after an HD session. Lesser degrees were observed in patients with non-dialysis-dependent chronic kidney disease. CD56 and CD161 NK cell marker expression was decreased in renal impairment. CD56(+) and CD161(+) iNKT cells produced more interferon-γ than negative cells of the same donor. Within the first year after kidney transplantation, the decrease in iNKT cells and their NK cell markers was reverted.
  
  
  CONCLUSIONS
  We describe for the first time that iNKT lymphocytes are reduced in end-stage renal disease and further depleted by HD. iNKT cells are important for early host response including activation of other immune cells and their depletion may contribute to immune dysfunction in renal disease.
authors.affiliation: Division of Nephrology and Hypertension, Department of Medicine, Hannover Medical School, Hannover, Germany.
authors.forename: Konrad
authors.initials: K
authors.lastname: Peukert
authors.forename: Gerhard
authors.initials: G
authors.lastname: Wingender
authors.forename: Margret
authors.initials: M
authors.lastname: Patecki
authors.forename: Stephan
authors.initials: S
authors.lastname: Wagner
authors.forename: Roland
authors.initials: R
authors.lastname: Schmitt
authors.forename: Shuwang
authors.initials: S
authors.lastname: Ge
authors.forename: Anke
authors.initials: A
authors.lastname: Schwarz
authors.forename: Mitchell
authors.initials: M
authors.lastname: Kronenberg
authors.forename: Hermann
authors.initials: H
authors.lastname: Haller
authors.forename: Sibylle
authors.initials: S
authors.lastname: von Vietinghoff
mesh_terms: D058186:Acute Kidney Injury / Q000276:immunology* / Q000601:surgery*; D000368:Aged; D015331:Cohort Studies; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D007371:Interferon-gamma / Q000378:metabolism; D016030:Kidney Transplantation; D008297:Male; D008875:Middle Aged; D055611:Natural Killer T-Cells / Q000276:immunology*; D020127:Recovery of Function; D006435:Renal Dialysis; D016176:T-Lymphocyte Subsets / Q000276:immunology*
chemical_list: D007371:Interferon-gamma
keywords: dialysis; end-stage renal disease; natural killer T cells; specific immunity