616 Peripheral natural killer (NK) cells are depleted and functionally impaired in chronic HCV infection

Golden–Mason, Lucy; Asrafel, Hameda; Rosen, Hugo R.; Madrigal-Estebas, Laura; Doherty, Derek G.; Hegarty, John E.

doi:10.1016/s0270-9139(03)80658-4

Cited by 2 publications

(3 citation statements)

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“…In agreement with others, we found that CD3 -CD56 + NK cells are decreased in HCV-infected patients [6,27]. Furthermore, we found that without PEG-IFN-a-2b stimulation, HCV-infected patients had fewer activated NK cells, activated bright (CD3 -CD56 +bright CD69 + ) and activated dim (CD3 -CD56 +dim CD69 + ) NK cells compared to controls, suggesting that chronic HCV infection may alter both the immunoregulatory and the cytotoxic function of NK cells.…”

Section: Discussionsupporting

confidence: 93%

“…In vitro, HCV core protein can up-regulate major histocompatibility complex (MHC) class I expression resulting in significantly down-regulated NK cytotoxic activity [32]. We also evaluated CD3 -CD161 + cells and found that CD161 expression did not differ between any of our patient groups (data not shown), corroborating results from others [27], suggesting that changes in CD161 expression are not associated with HCV clearance.…”

Section: Discussionsupporting

confidence: 87%

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CD56+dim and CD56+bright cell activation and apoptosis in hepatitis C virus infection

Lin¹,

Gonzalez²,

Cunningham‐Rundles

et al. 2004

Clinical and Experimental Immunology

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SUMMARY 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)-a . 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)-a -2b. A subset of HCV-infected patients, subsequently treated with PEG-IFN-a -2b in vivo , was determined to have a sustained virological response (SVR, n = 6) or to not respond (NR) to treatment ( n = 5). In the absence of IFN, activated dim (CD3 -CD56 +dim CD69 + ) NK cells were significantly decreased ( P = 0·04) while activated apoptotic dim (CD3 -CD56 +dim CD69 + annexin-V + ) NK cells tended to be increased ( P = 0·07) in SVR patients compared with NR patients. Activated bright (CD3 -CD56 +bright CD69 + ) and activated apoptotic bright (CD3 -CD56 +bright CD69 + annexin-V + ) NK cells were significantly correlated ( P = 0·02 and P = 0·01, respectively) with increasing hepatic inflammation. These findings suggest that in the absence of PEG-IFN, activated dim (CD3 -CD56 +dim CD69 + ) NK cell turnover may be enhanced in SVR compared with NR patients and that activated bright (CD3 -CD56 +bright CD69 + ) NK cells may play a role in liver inflammation.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionsupporting

confidence: 87%

CD56+dim and CD56+bright cell activation and apoptosis in hepatitis C virus infection

Lin¹,

Gonzalez²,

Cunningham‐Rundles

et al. 2004

Clinical and Experimental Immunology

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show abstract

“…Several groups have demonstrated that liver CD56 + CD3 -NK cells and CD56 + CD3 + NKT cells decrease in parallel with the histologic progression of HCV, and in cirrhotic livers are further diminished in numbers, ability to secrete IFN-γ , and cytotoxicity (eg, killing of K562, Raji cells, and human hepatoma cell line) [19][20][21]. In addition, our collaborators have recently found that circulating NK cells are also decreased and functionally impaired in active chronic HCV [22].…”

Section: Nk and Nkt Cellsmentioning

confidence: 99%

Immunity and persistence in hepatitis C virus infection

Wertheimer

Rosen²

2003

Curr hepatitis rep

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616 Peripheral natural killer (NK) cells are depleted and functionally impaired in chronic HCV infection

Cited by 2 publications

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CD56+dim and CD56+bright cell activation and apoptosis in hepatitis C virus infection

CD56+dim and CD56+bright cell activation and apoptosis in hepatitis C virus infection

Immunity and persistence in hepatitis C virus infection

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