Dim (CD3 −CD56 +dim CD16 +) NK cells are cytolytic and comprise more than 90% of CD3 −CD56 + NK cells, whereas bright (CD3 −CD56 +bright CD16 −) NK cells are immunoregulatory principally through cytokine production. NK cells can be divided into two subsets, dim and bright, according to CD56 surface density expression.
These findings suggest that in the absence of PEG-IFN, activated dim (CD3 −CD56 +dimCD69 +) NK cell turnover may be enhanced in SVR compared with NR patients and that activated bright (CD3 −CD56 +brightCD69 +) NK cells may play a role in liver inflammation.ĬD56 + natural killer (NK) cells, which comprise approximately 10% of human peripheral blood mononuclear cells (PBMCs) and up to 30% of intrahepatic mononuclear cells, are critical for innate antiviral host defence since these cells have the capacity to limit viremia before adaptive T and B cell antigen-specific responses emerge. Activated bright (CD3 −CD56 +brightCD69 +) and activated apoptotic bright (CD3 −CD56 +brightCD69 +annexin-V +) NK cells were significantly correlated ( P = 0♰2 and P = 0♰1, respectively) with increasing hepatic inflammation. In the absence of IFN, activated dim (CD3 −CD56 +dim CD69 +) NK cells were significantly decreased ( P = 0♰4) while activated apoptotic dim (CD3 −CD56 +dimCD69 +annexin-V +) NK cells tended to be increased ( P = 0♰7) in SVR patients compared with NR patients. A subset of HCV-infected patients, subsequently treated with PEG-IFN- α-2b in vivo, was determined to have a sustained virological response (SVR, n = 6) or to not respond (NR) to treatment ( n = 5). We used flow cytometry to enumerate activated (CD69 +) and apoptotic (annexin-V +) dim (CD3 −CD56 +dim) and bright (CD3 −CD56 +bright) NK cells obtained from HCV-infected patients before treatment ( n = 16) and healthy controls ( n = 15) in the absence and presence of pegylated interferon (PEG-IFN)- α-2b. CD3 −CD56 +dim natural killer (NK) cells, which are cytotoxic against virally infected cells, may be important in hepatitis C virus (HCV)-infected patients who are successfully treated with pegylated interferon (PEG-IFN)- α.
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