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BukuDifferential CD4+ and CD8+ T-Cell Responsiveness in Hepatitis C Virus Infection (from Hepatology 2001, 33(1), 267-276)
Bibliografi
Author: Chang, Kyong-Mi ; Thimme, Robert ; Melpolder, Jacqueline J. ; Oldach, David ; Pemberton, Janell ; Moorhead-Loudis, Jacquelyn ; McHutchison, John G. ; Alter, Harvey J. ; Chisari, Francis V.
Topik: HCV; Hepatitis C; Validation ref - 6
Bahasa: (EN )    
Penerbit: American Association for the Study of Liver Disease     Tahun Terbit: 2001    
Jenis: Article - diterbitkan di jurnal ilmiah internasional
Fulltext: Chang_et_al-2001-Hepatology.pdf (296.91KB; 0 download)
Abstract
This study was performed to compare the vigor and phenotype of virus-specific CD41 and CD81 T-cell responses in patients with different virologic and clinical outcomes after hepatitis C virus (HCV) infection. The results show that a vigorous and multispecific CD41 proliferative T-cell response is maintained indefinitely after recovery from HCV infection whereas it is weak and focused in persistently infected patients. In contrast, the HCV-specific CD81 T-cell response was quantitatively low in both groups despite the use of sensitive direct ex vivo intracellular interferon gamma (IFN-g) staining. Furthermore, although HCV-specific cytolytic CD81 memory T cells were undetectable ex vivo, they were readily expanded from the peripheral blood of chronically HCV-infected patients but not from recovered subjects after in vitro stimulation, suggesting that ongoing viremia is required to maintain the HCV-specific memory CD81 T-cell response. HCV-specific CD81 T cells displayed a type 1 cytokine profile characterized by production of IFN-g despite persistent HCV viremia. The paradoxical observation that HCV-specific CD41 T cells survive and CD81 T cells are lost after viral clearance while the opposite occurs when HCV persists suggests the existence of differential requirements for the maintenance of CD41 and CD81 T-cell memory during HCV infection. Furthermore, the relative rarity of circulating CD81 effector T cells in chronically infected patients may explain the chronic insidious nature of the liver inflammation and also why they fail to eliminate the virus.

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