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*
First Department of Medicine and
Department of General Medicine, Osaka University Medical School, Suita, Japan
In hepatitis C virus (HCV) infection, Th responses are implicated
in the pathogenesis of liver disease. The dendritic cell (DC) is the
most potent activator of CD4 T cells for supporting Th1
differentiation. To clarify the roles of DC of HCV-infected individuals
in the development of CD4 T cell responses, we generated peripheral DC
with GM-CSF and IL-4 from 24 chronic hepatitis C patients and 14
healthy donors. We then compared their potentials for stimulating
allogeneic CD4 T cells, autologous CD4 T cells against influenza A or
HCV core Ags, and cytokine production. The DC from the patients
(HCV-DC) expressed lower degrees of CD86 than DC from the donors
(N-DC), whereas no difference was found in the HLA molecules and other
costimulators. HCV-DC stimulated allogeneic T cells less than N-DC;
however, influenza A- or core-pulsed HCV-DC retained the potentials for
autologous T cell proliferation. In allogeneic DC/T cell cultures, the
IFN-
levels with HCV-DC were lower than those with N-DC, which may
be related to the low expressions of IL-12 p35 and p40 transcripts in
HCV-DC. The stimulation with LPS disclosed that HCV-DC is less potent
in IL-12 p70 production than N-DC. In the autologous cultures, the
pulsing of the Ags to HCV-DC increased the IL-12 p40 and IFN-
production and up-regulated the transcription of both IL-12 subunits.
Exogenous IL-2 or IL-12 restored the low allogeneic T cell
proliferation with HCV-DC in a dose-dependent manner. Therefore, low
expression of CD86 and/or IL-12 is crucially involved in the low
allostimulatory capacity of HCV-DC. Low IL-12 and low IFN- milieu
with HCV-DC on encounters with alloantigens may impede Th1
polarization.
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