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BukuHepatic expansion of a virus-specific regulatory CD8+ T cell population in chronic hepatitis C virus infection (from The Journal of Clinical Investigation, Vol. 113 (7), April 2004)
Bibliografi
Author: Accapezzato, Daniele ; Francavilla, Vittorio ; Paroli, Marino ; Casciaro, Marco ; Chircu, Lucia Valeria ; Cividini, Agostino ; Abrigani, Sergio ; Mondelli, Mario U. ; Barnaba, Vincenzo
Topik: HCV; Hepatitis C; CD8+ T cell; Validation ref - 2
Bahasa: (EN )    
Tahun Terbit: 2004    
Jenis: Article - diterbitkan di jurnal ilmiah internasional
Fulltext: JCI0420515.pdf (740.93KB; 0 download)
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Abstract
Hepatitis C virus (HCV) is capable of persisting in the host to establish a lifelong liver disease in the majority of infected individuals (reviewed in ref. 1). The high propensity of HCV to establish persistent
infection has been related to a severe dysfunction of HCVspecific CD8+ CTLs, which seems to be a critical factor in preventing resolution of infection and in favoring the onset of chronic liver immunopathology (1–11). In addition, further data indicated inefficient CTLs in both HCV-related and -unrelated chronic infections, suggesting that this phenotype is not restricted to HCV but is widely present in persistent viral infections (4, 12–17). However, the studies conducted thus far have not addressed the issues of why the expansion of HCV-specific CTL populations contrasts with their poor capacity to perform immediate effector functions or whether intrahepatic T cell populations have particular subsets involved in the establishment of chronic infection. Recently, a large body of evidence has indicated that different types of both CD4+ and CD8+ regulatory T (TR) cells, once activated, possibly in an antigen-specific manner, suppress excessive effector responses in an antigen-specific or a -nonspecific manner (18–24). This equilibrium may establish a status of long-lasting low-level inflammation critical to the survival of both the microbial agent and the host.
Here we report that patients with chronic HCV infection show a considerable enrichment of HCV-specific CTLs in the liver (in contrast to what is observed in the periphery) that express the tissuehoming phenotype of memory effector (ME) cells (CCR7–) (25), despite the fact that only a minority of these CTLs carry out prompt proinflammatory functions. Importantly, we demonstrate the concomitant presence in the liver of HCV-specific CTLs producing IL-10 that appear to have regulatory functions and thus have a major role in the establishment of the long-lasting low-level liver inflammation.

[validation ref - 2]
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