O. Delpuech et al., The hepatitis C virus (HCV) induces a long-term increase of interleukin-10production by human CD4(+) T cells (H9), EUR CYTOKIN, 12(1), 2001, pp. 69-77
Patients with chronic hepatitis C present an imbalance of Th1/Th2 cytokine
production. Therefore, we investigated whether the exposure of the CD4(+) T
cell line H9 to HCV could induce activation of cells through synthesis of
IL-10.
Three infection protocols were performed to enhance HCV propagation. Viral
particles were prepared by ultracentrifugation of serum from patients. From
3 to 81 days post-infection (p,i.), HCV-RNA was monitored both in supernat
ants and cells by nested RT-PCR, IL-10 protein in medium by ELISA, and IL-1
0 mRNA in cells by semi-quantitative RT-PCR, The expression of tetraspanins
was analyzed by flow cytometry, The PKC signal pathway was studied using s
pecific inhibitors. The H9 cells express CD81, HCV-RNA (+) was detected in
cells until 21 days p,i, and in culture media over 39 days p,i, Up to day 8
1 p,i,, HCV exposure induced a specific, 2-fold increase of IL-10 productio
n by H9 cells. IL-IO production was inhibited by a PKC inhibitor (Calphosti
n C), This study shows that even if the infection of H9 T cells did not res
ult in any viral progeny, HCV induced the activation of IL-10 secretion, wh
ich supports the role of IL-10 in HCV pathogenesis.