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Subversion of effector CD8+ T cell differentiation in acute hepatitis C virus infection: exploring the immunological mechanisms

Item Type:Article
Title:Subversion of effector CD8+ T cell differentiation in acute hepatitis C virus infection: exploring the immunological mechanisms
Creators Name:Francavilla, V. and Accapezzato, D. and De Salvo, M. and Rawson, P. and Cosimi, O. and Lipp, M. and Cerino, A. and Cividini, A. and Mondelli, M.U. and Barnaba, V.
Abstract:Hallmark of acute hepatitis C virus (HCV) infection is a severe virus-specific effector CD8+ T cell dysfunction that seems to be a critical factor in preventing the resolution of infection and in favoring the onset of chronic liver immunopathology. We suggest that this dysfunction is critical in the establishment of HCV persistence, unless it is compensated by multispecific responses, as found in individuals resolving infection. Analyses on purified populations indicate that central memory HCV-specific CCR7+/CD8+ T cells efficiently proliferate and differentiate in vitro, although the large population of memory effector CCR7- cells found in the peripheral blood of acutely infected patients display poor effector functions ex vivo (semi-effectors). However, we report strong evidence in support of IL-2 being capable of pushing semi-effector CTL to complete their effector cell program. Therefore, IL-2 deficiency during T cell activation may be responsible for the dichotomy between memory CTL expansion and incomplete effector differentiation shown in patients with acute HCV infection. These data are consistent with the possible therapeutic treatment with IL-2 to rebuild the effector T cell pool in these patients.
Keywords:Cellular Activation, Cellular Differentiation, CTL, Memory
Source:European Journal of Immunology
ISSN:0014-2980
Publisher:Wiley (U.S.A.)
Volume:34
Number:2
Page Range:427-437
Date:1 January 2004
Official Publication:https://doi.org/10.1002/eji.200324539
PubMed:View item in PubMed

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