title: Compromised function of natural killer cells in acute and chronic viral hepatitis.
abstract: BACKGROUND
  Natural killer (NK) cells are an integral part of the innate immune system. They have been suggested to play an important role in both defense against viral hepatitis and the pathogenesis of other liver diseases.
  
  
  METHODS
  NK cells from 134 individuals including patients with acute hepatitis B and C as well as chronic hepatitis B, C, and delta (D) patients were studied.
  
  
  RESULTS
  Infection with viral hepatitis was associated with increased frequencies of NK cells in the peripheral blood; that NK cells showed a less activated phenotype and were compromised in cytolotytic function and cytokine production in all viral hepatitis infections: Hepatitis virus infections did not alter NK cell differentiation, and the activity and severity of liver disease were reflected by alterations of NK cell surface receptors as demonstrated by principal component analysis.
  
  
  CONCLUSIONS
  NK cell phenotypic and functional alterations can equally be observed in HBV, HCV, and HDV infections. Instead, patterns of NK cell alterations differ in acute and chronic infections. Thus, our data suggest a common mechanism in the alteration of NK cell phenotype and function with unique variations that depend on disease activity rather than virus-specific factors.
authors.affiliation: Department of Gastroenterology, Hepatology and Endocrinology, Hannover Medical School, Hannover, Germany.
authors.forename: Sebastian
authors.initials: S
authors.lastname: Lunemann
authors.forename: David F G
authors.initials: DF
authors.lastname: Malone
authors.forename: Julia
authors.initials: J
authors.lastname: Hengst
authors.forename: Kerstin
authors.initials: K
authors.lastname: Port
authors.forename: Jan
authors.initials: J
authors.lastname: Grabowski
authors.forename: Katja
authors.initials: K
authors.lastname: Deterding
authors.forename: Antoaneta
authors.initials: A
authors.lastname: Markova
authors.forename: Birgit
authors.initials: B
authors.lastname: Bremer
authors.forename: Verena
authors.initials: V
authors.lastname: Schlaphoff
authors.forename: Markus
authors.initials: M
authors.lastname: Cornberg
authors.forename: Michael P
authors.initials: MP
authors.lastname: Manns
authors.forename: Johan K
authors.initials: JK
authors.lastname: Sandberg
authors.forename: Hans-Gustaf
authors.initials: HG
authors.lastname: Ljunggren
authors.forename: Niklas K
authors.initials: NK
authors.lastname: Björkström
authors.forename: Heiner
authors.initials: H
authors.lastname: Wedemeyer
mesh_terms: D000208:Acute Disease; D000328:Adult; D000368:Aged; D015703:Antigens, CD / Q000097:blood / Q000276:immunology; D016022:Case-Control Studies; D005260:Female; D006521:Hepatitis, Chronic / Q000097:blood / Q000276:immunology* / Q000503:physiopathology; D006801:Humans; D007694:Killer Cells, Natural / Q000276:immunology* / Q000473:pathology; D008297:Male; D008875:Middle Aged; D010641:Phenotype; D025341:Principal Component Analysis; D055815:Young Adult
chemical_list: D015703:Antigens, CD
keywords: HBV; HCV; HDV; NK cells; viral hepatitis