Differential alteration of CD56(bright) and CD56 (dim) natural killer cells in frequency, phenotype, and cytokine response in chronic hepatitis C virus infection.

<bold>Background: </bold>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.<bold>Methods: </bold>We investigated the frequency, phenotype, and cytokine response of these subsets in blood from CHC patients and healthy subjects (HS).<bold>Results: </bold>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.<bold>Conclusions: </bold>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. [ABSTRACT FROM AUTHOR]