title: Differential alteration of CD56(bright) and CD56 (dim) natural killer cells in frequency, phenotype, and cytokine response in chronic hepatitis C virus infection.
abstract: BACKGROUND
  Natural killer (NK) cells play an important role in immune responses to virus infection. The cell population consists of CD56(bright) (bright-subset) and CD56(dim) (dim-subset) subsets that possess armed functions of cytokine production and cytolysis, respectively. How these subsets are involved in chronic hepatitis C virus infection (CHC) remains obscure.
  
  
  METHODS
  We investigated the frequency, phenotype, and cytokine response of these subsets in blood from CHC patients and healthy subjects (HS).
  
  
  RESULTS
  Dim-subset, but not bright-subset, showed lower frequency in the patients than in HS. Bright-subset from the patients more frequently expressed the NKG2A/CD94 inhibitory receptor than that from HS, while both subsets from the patients expressed lower levels of the NKG2D activating receptor. Both subsets from the patients displayed a significantly higher level of the signal transducer and activator of transcription (STAT) 1, compared with the HS. Upon stimulation with interferon-α, bright-subset activated less STAT4, required for interferon-γ production, and dim-subset activated more STAT1, required for cytolysis, in the patients than in HS.
  
  
  CONCLUSIONS
  These results indicate alterations of NK cell subsets in frequency, phenotype, and cytokine response in CHC, which might be associated with the immune pathogenesis of CHC.
authors.affiliation: Department of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, Yamada-oka, Suita, Osaka, Japan.
authors.forename: Takuya
authors.initials: T
authors.lastname: Miyagi
authors.forename: Satoshi
authors.initials: S
authors.lastname: Shimizu
authors.forename: Tomohide
authors.initials: T
authors.lastname: Tatsumi
authors.forename: Kumiko
authors.initials: K
authors.lastname: Nishio
authors.forename: Naoki
authors.initials: N
authors.lastname: Hiramatsu
authors.forename: Tatsuya
authors.initials: T
authors.lastname: Kanto
authors.forename: Norio
authors.initials: N
authors.lastname: Hayashi
authors.forename: Tetsuo
authors.initials: T
authors.lastname: Takehara
mesh_terms: D000328:Adult; D000368:Aged; D019002:CD56 Antigen / Q000378:metabolism*; D055612:Cytokine-Induced Killer Cells / Q000276:immunology / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism; D005260:Female; D019698:Hepatitis C, Chronic / Q000097:blood / Q000276:immunology*; D006801:Humans; D007694:Killer Cells, Natural / Q000276:immunology* / Q000378:metabolism; D008213:Lymphocyte Activation; D018655:Lymphocyte Count; D016131:Lymphocyte Subsets / Q000276:immunology* / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D055655:NK Cell Lectin-Like Receptor Subfamily K / Q000378:metabolism; D010641:Phenotype; D050794:STAT1 Transcription Factor / Q000378:metabolism; D050797:STAT4 Transcription Factor / Q000378:metabolism
chemical_list: D019002:CD56 Antigen; D016207:Cytokines; D055655:NK Cell Lectin-Like Receptor Subfamily K; D050794:STAT1 Transcription Factor; C494079:STAT1 protein, human; D050797:STAT4 Transcription Factor; C494090:STAT4 protein, human